New Evidence in the Management of Chronic

Hypertension in Pregnancy

Tiina Podymow, MD,* and Phyllis August, MD, MPH†

Summary: Chronic hypertension complicates 1% to 5% of all pregnancies, but debate continues regarding the
benefits of lowering blood pressure in pregnancy as well as the optimal blood pressure targets. Women with
chronic hypertension are at significant risk for maternal and fetal morbidity and mortality, yet it remains unclear
whether antihypertensive treatment during pregnancy lowers these risks. Severe hypertension (systolic Z 160
mm Hg) should be treated, but there is considerable variability in the approach to mild-to-moderate
hypertension (140-159/90-109 mm Hg). The recently published CHIPS (Control of Hypertension in Pregnancy
Study) trial is an important effort to attempt to determine treatment goals in mild to moderate pregnancy
hypertension. The risks and benefits of tight versus less tight control of blood pressure in nonproteinuric
hypertensive women, most of whom had pre-existing hypertension, were evaluated. A main finding was an
increased risk of severe hypertension (adjusted odds ratio, 1.8) when blood pressure was not tightly controlled.
In this review, general management of chronic hypertension in pregnancy is discussed, including changes in
treatment that may be appropriate in light of new clinical trial data.
Semin Nephrol 37:398-403 C 2017 Elsevier Inc. All rights reserved.
Keywords: chronic hypertension, hypertension, pregnancy, preeclampsia, guidelines, hypertension,
antihypertensives, postpartum hypertension

C
hronic hypertension, defined as blood pressure
(BP) 4 140/90 mm Hg prior to 20 weeks, or a
known diagnosis of hypertension preceding to
pregnancy, complicates 1% to 5% of all pregnancies,1,2
and the risks to both the mother and the baby are well
documented. Adverse outcomes for both the mother and
the baby are far more common in chronically hyper-
tensive compared to normotensive pregnancies. Super-
imposed preeclampsia develops in 25% to 30% of
chronically hypertensive mothers,3 and preeclampsia is
considered the most important cause of indicated prema-
turity. Risk of early (o 37 weeks) delivery in chronically
hypertensive women was found to be increased by 3-fold
in a recent meta-analysis of US studies.3 Additional risks
to the fetus include growth restriction (birthweight
o 10th percentile), which occurs in 5% to 13% of
infants born to chronically hypertensive mothers.4 Babies
born to women with preeclampsia are at increased risk for
respiratory complications and may require high-level
neonatal care,5,6 and there is a 4-fold increased risk of
perinatal death.3 For chronically hypertensive women, in
addition to preeclampsia, antenatal complications include
uncontrolled hypertension, which may require hos-
*
Division of Nephrology, McGill University Health Centre, Mon-
treal, Canada.
†
Division of Nephrology and Hypertension, Weill Cornell Medical
College, Cornell University, New York, NY.
Financial disclosure and conflict of interest statements: none.
Address reprint requests to Tiina Podymow, MD, McGill University
Health Centre, Royal Victoria Hospital, Glen Site D05-7176,
1001 boul Decarie, Montreal, QC H4A 3J1, Canada. E-mail:
tiina.podymow@muhc.mcgill.ca
0270-9295/ - see front matter
& 2017 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.semnephrol.2017.05.012
pitalization. Postpartum, women may develop severe
hypertension and are at risk for transient ischemic attack,
stroke, pulmonary edema, and acute kidney injury.5
APPROACH TO CHRONIC NONPROTEINURIC
HYPERTENSION IN PREGNANCY
Preconception is the appropriate time to discuss the risks
of hypertension in pregnancy. There is a high likelihood
of a favorable outcome with risks, nonetheless, in the
range of 25% for development of superimposed pre-
eclampsia. In early pregnancy, routine laboratory tests,
including those associated with preeclampsia such as
uric acid, platelets, liver function tests, creatinine, and
urine protein-to-creatinine ratio, should be performed as
a baseline to determine the clinical significance if
preeclampsia is suspected in later pregnancy. Patient
compliance is essential because home BP monitoring as
well as frequent clinic visits will increase the likelihood
of detecting preeclampsia and other complications
before they become life threatening.
Medications with deleterious fetal effects, such as
angiotensin-converting enzyme inhibitors and angioten-
sin II receptor antagonists, should be addressed, and it
must be understood by the patient that they be discon-
tinued as soon as pregnancy is diagnosed.7 With regard
to nonpharmacologic management, in pregnancy there is
a departure from accepted guidelines for nonpregnant
hypertensive patients, in that lifestyle changes including
exercise, weight loss, and low-salt diet are not advised.
Secondary Hypertension
Although most women with chronic or preexisting
hypertension have essential hypertension, it is important

398 Seminars in Nephrology, Vol 37, No 4, July 2017, pp 398–403

New evidence in the management of pregnancy hypertension 399

Special studies

Results

Figure 1. Algorithm for diagnosis and treatment of secondary hypertension in pregnancy. *Serum and urine.
§Renin, urine aldosterone, urine potassium; difficult to interpret in pregnancy. Renal evaluation: serologic
evaluation, 24-h urine, renal ultrasound. Renovascular tests: renin (normally elevated in pregnancy) Doppler
ultrasound of renal arteries, magnetic resonance imaging (MRI). Abn, abnormal; BP, blood pressure; CPAP,
continuous positive airway pressure treatment under care of a respirologist; DM, diabetes mellitus; HTN,
hypertension prescription treatment; Med, medical; pheo, pheochromocytoma; r/o, ; Rx, prescription; SLE,
systemic lupus erythematosus.

to consider the possibility of secondary hypertension.
Young women with hypertension may be somewhat
more likely (compared with middle-aged women) to
have secondary hypertension (eg, intrinsic renal disease,
renovascular hypertension, primary aldosteronism, Cush-
ing syndrome, pheochromocytoma, obstructive sleep
apnea). When this is suspected, noninvasive evaluation
may be appropriate (Fig. 1).
Prevention of Preeclampsia
Although an important goal of management, there is as
yet, no “magic bullet” to prevent preeclampsia. Aspirin
has been extensively studied and has been shown to be
safe; the mechanism of action may be the reversal of
the imbalance between prostacyclin and thromboxane,
and its antiplatelet effects. Large trials and several meta
analyses suggest that although the benefit may be
modest, in women with significant risk, low-dose
aspirin is associated with approximately 10% to 20%
lower risk of preeclampsia compared with placebo.8
This will be reviewed more in detail in the “Pree-
clampsia: Pathogenesis, Prevention, and Long-Term
Complications” article in this special issue.
Pharmacologic Management
BP normally falls in early pregnancy including in women
with chronic hypertension, and if there is no known target
organ damage clinicians can consider discontinuing
antihypertensive treatment and monitoring. Our strategy
is to initiate therapy at a BP of 140 to 150/90 to 100 mm
Hg regardless of the type of hypertension.9 There are a
variety of agents available for use (Table 1),10 and orally
administered antihypertensive agents should be used in
standard doses in pregnancy.
Thresholds for Initiating Medication and Treatment
Targets
The guidelines from the societies of obstetric medicine
(American, Canadian, Australia/New Zealand, and
European) all agree to treat pregnancy hypertension if
BP is elevated to greater than or equal to 160/105 to
110 mm Hg11 because of the concern of increased risk of
pregnancy-associated stroke when systolic BP is greater
than 160 mm Hg.12 Additionally, there is agreement to
normalize BP (to o 140/90 mm Hg) in women with end
organ dysfunction, for example in those with proteinuric
renal disease. The debate arises in treatment of nonsevere
chronic hypertension without comorbid conditions,
wherein BP targets in pregnancy are debated: will
maternal BP targets that are too low worsen risk of
intrauterine growth restriction?13 Will too-high targets
result in uncontrolled hypertension or preeclampsia? To
answer this last point, a 2014 Cochrane review concluded
that treatment of mild-moderate hypertension in preg-
nancy halved the risk of uncontrolled hypertension;
however, there was not enough evidence to show if
treatment of mild-moderate hypertension prevented
400 T. Podymow and P. August

Table 1. Drugs for Gestational or Chronic Hypertension in Pregnancy

Drug (FDA risk*) Dose Concerns or Comments
Preferred agent 0.5-3.0 g/d in 2-3 Drug of choice according to NHBEP working group; safety after first
Methyldopa (B) divided doses trimester well documented, including 7-year follow-up of offspring
Second-line agents† 200-1200 mg/d in 2-3 Labetalol is one of the preferred agents in the treatment of chronic
Labetalol (C) divided doses hypertension in pregnancy. Beta-blockers as a class may be associated
with fetal growth restriction and neonatal bradycardia. Avoid in asthma.
Nifedipine (C) 30-90 mg/d of a slow- Nifedipine is one of the preferred agents in the treatment of chronic
release preparation hypertension in pregnancy. Less experience with other calcium entry
blockers.
Hydralazine (C) 50-300 mg/d in 2-4 Few controlled trials, long experience with few adverse events
divided doses documented; useful only in combination with sympatholytic agent. May
cause neonatal thrombocytopenia.
β receptor blockers (C) Depends on specific May cause fetal bradycardia and decrease uteroplacental blood flow, this
agent effect may be less for agents with partial agonist activity. May impair
fetal response to hypoxic stress; risk of growth retardation when started
in first or second trimester (atenolol).
Hydrochlorothiazide (B) 25 mg/d Majority of controlled studies in normotensive pregnant women rather than
hypertensive patients; can cause volume depletion and electrolyte
disorders.
Contraindicated in — Women should stop ACEIs in first trimester/when pregnancy is diagnosed;
second and third the finding of teratogenic effects for first trimester exposure may be
trimesters confounded by maternal disease.7 In second and third trimesters
ACEIs and angiotensin ACEIs/ARBs leads to fetal loss in animals; human use associated with
receptor antagonists (D) cardiac defects, fetopathy, renal agenesis, oligohydramnios, growth
restriction, and neonatal anuric renal failure.

Of note, no antihypertensive has been proven safe for use during the first trimester.
ACEIs, angiotensin-converting enzyme inhibitors; ARBs, angiotensin II receptor blockers.
*US Food and Drug Administration (FDA) classification.
†
We omit some agents (eg, clonidine, α-blockers) due to limited data on use for chronic hypertension in pregnancy.

preeclampsia.6 Treatment initiation and recommended BP
treatment goals differ widely among the various obstetric
societies (Table 2),11,14 and this has been confusing for
clinicians. For example, one clinician notes the illogic of
managing BP expectantly at less than 160/110 mm Hg
and then emergently at greater than 160/110 mm Hg.15
Guidelines have been generated by expert opinion and
have thus far been informed by small trials only.6
The CHIPS Trial and Subanalyses
The CHIPS (Control of Hypertension in Pregnancy
Study) is the first large randomized trial to attempt to
answer the clinical questions regarding treatment
targets in chronic nonproteinuric hypertension. The
CHIPS trial was an international, unblinded, multi-
center, randomized, controlled trial analyzing 987
women at 14þ0 to 33þ6 weeks with chronic hyper-
tension or gestational hypertension. Women with office
diastolic BP 90 to 105 mm Hg (85-105 if already on
antihypertensive agents) were randomized to either a
less tight (target diastolic BP 100 mm Hg) or a tight
(target diastolic BP 85 mm Hg) control group and were
analyzed with respect to maternal, fetal, and neonatal
outcomes.16 Exclusion criteria included multiple
gestations, major fetal anomalies, or the use of
angiotensin-converting enzyme inhibitors at greater
than 14 weeks gestation.
Seventy-five percent of the women had chronic
hypertension whereas 25% had gestational hyperten-
sion. Enrollment was at a mean of 24 weeks gestation,
and at baseline, the groups were well balanced.
Slightly more than half of the patients were taking
antihypertensive medication at enrollment, over one-
third were using home BP monitoring, and in a third
aspirin had been prescribed antenatally. Postrandom-
ization, labetalol was the recommended antihyperten-
sive of first choice, but this was not mandatory, and
labetalol, nifedipine, and methyldopa were most com-
monly used in the trial.
Outcomes were reported for 987 women; the pri-
mary outcome was a composite of pregnancy loss or
high-level neonatal care and serious maternal compli-
cations (preeclampsia, severe maternal hypertension
4 160/110 mm Hg) within gestation or the first 28
days postpartum. The trial was not powered to detect
differences in the frequency of fetal or maternal deaths,
nor was it a preeclampsia prevention trial. Secondary
outcomes included serious maternal complications (eg,
severe maternal hypertension), occurring up to 6 weeks
New evidence in the management of pregnancy hypertension 401

Table 2. Blood Pressure Targets11

When to Start Treatment Treatment Goals
ACOG 25
Z 160/105 for chronic HTN 120-160/80-105 for chronic HTN
OR
160/110 for gestational HTN or preeclampsia
SOGC26 BP lowered to o 160/110 in severe HTN 130-155/80-105 for nonsevere hypertension without
comorbid conditions*
OR OR
BP of 140-159/90-109 for nonsevere HTN with o140/90 nonsevere hypertension with comorbid
comorbid conditions conditions
NICE (www.guidance. 4 150/100 for uncomplicated chronic HTN/ o 150/100, but diastolic 4 80 for chronic
nice.org.uk) gestational HTN/preeclampsia hypertension
OR OR
4 140/90 for target-organ damage secondary to o 150/80-100, for gestational hypertension and
chronic HTN preeclampsia
SOMANZ27 Z 160/110 for mild-to-moderate HTN None recommended
OR
Z 170/110 for severe HTN
ISSHP28 160-170/110 for preeclampsia None recommended

Numbers indicate systolic blood pressure/diastolic blood pressure in mm Hg.

ACOG, American College of Obstetrics and Gynecology; HTN, hypertension; ISSHP, International Society for the Study of
Hypertension in Pregnancy; NICE, National Institute for Health and Care Excellence; RCOG, Royal College of Obstetricians and
Gynecologists; SOGC, Society of Obstetricians and Gynecologists of Canada; SOMANZ, Society of Obstetric Medicine of Australia
and New Zealand.
Reprinted with permission from Phipps et al.11
*Comorbid conditions: pregestational type I or II diabetes mellitus or kidney disease.

postpartum. BP readings in the groups were well
differentiated from randomization until delivery. As
expected BP was higher among women randomized to
less tight control: a mean of 5.8 mm Hg higher for
systolic BP and a mean 4.6 mm Hg for diastolic BP
(both P o .001 compared with tight control) with the
mean diastolic BP being 85.3 compared to 89.9 mm
Hg in the tight arm versus the less tight arm. There
were no between-group differences in primary outcomes;
the incidence of the primary composite perinatal outcome
(pregnancy loss, high level neonatal care) was 31.4% in
the less tight group versus 30.7% in the tight control
group (adjusted odds ratio [aOR], 1.02; 95% confidence
interval, 0.77-1.35). Notably there was no difference in
small babies, but there was a trend toward birth weight
less than 10th percentile in the tight control arm, 19.7%
versus 16.1% (aOR, 0.78; 95% confidence interval, 0.56-
1.08). The trial, however, was not powered for this
outcome. Perinatal mortality also did not differ signifi-
cantly between groups. It was 2.8% in the less tight arm
and 2.3% in tight control arm.
There was no interaction between allocated treat-
ment and type of hypertension on the secondary out-
come; results for women with chronic and gestational
hypertension were similar. Elevated liver enzymes and
low platelet counts were twice as common in the less
tight control group, but the P value o .05 did not meet
the prespecified threshold for statistical significance of
o .001 for other outcomes. The main trial finding was
that severe hypertension (4 160/110 mm Hg) was
significantly more common in women receiving less
tight (versus tight) control at 40.6% versus 27.5%
(aOR, 1.8; P o .001). This was not accompanied by
an increase in the serious complications of hypertension
or stroke. There was no difference in the incidence of
preeclampsia in the groups (49.1% for less tight versus
45.7% for tight).
Choice of Antihypertensive Therapy
In general, the selection of specific antihypertensive
agents in pregnancy is challenging and requires bal-
ancing efficacy and adverse maternal and fetal
effects.10,17 To date, no drug has been shown to be
more efficacious with respect to preventing preeclamp-
sia or other complications of pregnancy. Interestingly,
a secondary analysis of the CHIPS cohort was per-
formed by the authors, comparing methyldopa-treated
and labetalol-treated women for the same primary and
secondary outcomes as the main trial.18 Mixed-effects
logistic regression was used to compare outcomes, and
the main findings showed that women treated with
methyldopa (versus labetalol) had fewer adverse peri-
natal and maternal outcomes, including fewer babies
who were small for gestational age, and fewer mothers
with severe hypertension, preeclampsia and delivery at
less than 34 and less than 37 weeks. The use of
methyldopa appeared especially beneficial for women
402
with pre-existing hypertension. In a further secondary
logistic regression analysis, the results of CHIPS were
not found to be contingent on the choice of labetalol or
methyldopa to achieve maternal BP control.19 We
understand this to mean that clinicians may use either
methyldopa or labetalol to treat nonsevere hyperten-
sion, and that in many areas where only methyldopa
(but not labetalol) is available, treatment with methyl-
dopa can be considered optimal and standard of care.
WHAT HAVE WE LEARNED FROM THE CHIPS
TRIAL?
The CHIPS trial authors conclude that in the pregnan-
cies of chronically hypertensive women and women
with gestational hypertension the advantage of tighter
BP control is the significantly lower frequency of
severe maternal hypertension. Although tight control
does not appear to confer any apparent benefit to the
fetus, it does not result in major risk to the fetus or
newborn either. These conclusions are in keeping with
a 2014 Cochrane review studying 49 trials and a total
of 4,723 randomized subjects that showed the risk of
developing severe hypertension is halved, with no
difference in small-for-gestation babies.6
The CHIPS trial was a pragmatic trial; the effectiveness
of treatment in such a trial is intended to be translatable to
clinical practice and practice guidelines. So far, adoption of
tight control for chronic hypertension in pregnancy has not
been wide spread. In a special report statement, the Society
for Maternal-Fetal Medicine (United States) concentrated
on the increased risk of small-for-gestational-age and
lower-birthweight babies, the report authors ironically
concentrate on 15 year-old data by the authors of the
CHIPS trial.20 They advocate making no changes to
current guidelines (ie, starting treatment when chronically
hypertensive women present in the severe range of BP).
We disagree with this approach, and are encouraged by the
lack of harm of the lower BP target in the CHIPS study
and the encouraging outcome of fewer episodes of severe
hypertension. We are concerned that severe hypertension is
a risk factor for cerebrovascular catastrophe, and although
rare, this outcome is devastating.
Looking forward, a large multicenter study of 4,700
chronically hypertensive women is underway in the United
States comparing a target BP of less than 140/90 mm Hg
with no treatment unless hypertension is in the severe
range. Enrollment is prior to or at 18 weeks gestation. The
study is set for completion in 2020 (ClinicalTrials.gov
NCT02299414).
Postpartum Follow-Up
Hypertension frequently persists after delivery in women
with antenatal hypertension. Women with chronic hyper-
tension who have developed superimposed preeclampsia
T. Podymow and P. August
are particularly at risk for significant elevations of
BP in the postpartum period. BP may increase even
higher if patients are treated with nonsteroidal
anti-inflammatory agents, and we recommend using
alternative peripartum analgesia. Most pregnancy-
associated strokes occur in the postpartum period,12
and hypertension should be treated aggressively and
BP carefully normalized. In most women it is appro-
priate to continue those oral antihypertensive agents
given antenatally in the postpartum period; however,
increased doses may be necessary. In preeclampsia
there may be reversal of diurnal BP rhythms with
hypertension worse at night,21,22 which can be helped
by dividing antihypertensive dosing to include a bed-
time dose. We recommend close follow-up in the
postpartum period for women with chronic hyper-
tension, as normalization may occur in the first weeks
or months postpartum, and as such, women may need
to use home BP monitors and medications may need
to be stopped. Close communication between the
patient and the treating physician is vital during this
period.23
Antihypertensive Medications and Lactation
Neonatal exposure to methyldopa, labetalol, captopril,
enalapril, and nifedipine via nursing are low, thus these
medications are considered safe in breastfeeding.24
Atenolol and metoprolol are concentrated in breast
milk, possibly to levels that could affect the infant, and
therefore are not recommended. Finally, although the
concentration of diuretics in breast milk is low, these
agents may reduce milk production due to mild volume
contraction, which may interfere with the ability to
successfully breast feed.
CONCLUSION
The variation in the approach to mild to moderate
pregnancy hypertension has been illuminated by the
CHIPS trial, which demonstrated benefit in targeting
BP values to what is recommended in nonpregnant
patients (ie, o140/90 mm Hg). Decreased risk of
severe hypertension was seen in women who were in
the tight control group. These results confirm previous
meta-analyses and demonstrate that lowering BP to this
target is safe for the fetus. The elevated risk of
preeclampsia in chronically hypertensive women
remains best mitigated by the use of aspirin, as the
data supporting BP control for preeclampsia prevention
are currently lacking. Methyldopa and labetalol were
used in the CHIPS trial and remain first-line options
when pharmacologic treatment is necessary, and opti-
mal management requires close cooperation and com-
munication among the patient, obstetrician, and the
maternal-fetal nephrologist/internist.
New evidence in the management of pregnancy hypertension
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