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1. Hypertension in pregnancy: Diagnosis and treatment.................................................................................. 1

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Hypertension in pregnancy: Diagnosis and treatment

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Abstrak: Hypertension affects 10% of pregnancies in the United States and remains a leading cause of both
maternal and fetal morbidity and mortality. Hypertension in pregnancy includes a spectrum of conditions, most
notably preeclampsia, a form of hypertension unique to pregnancy that occurs de novo or superimposed on
chronic hypertension. Risks to the fetus include premature delivery, growth retardation, and death. The only
definitive treatment of preeclampsia is delivery. Treatment of severe hypertension is necessary to prevent
cerebrovascular, cardiac, and renal complications in the mother. The 2 other forms of hypertension, chronic and
transient hypertension, usually have more benign courses. Optimal treatment of high blood pressure in
pregnancy requires consideration of several aspects unique to gestational cardiovascular physiology. The major
goal is to prevent maternal complications without compromising uteroplacental perfusion and fetal circulation.
Before an antihypertensive agent is prescribed, the potential risk to the fetus from intrauterine drug exposure
should be carefully reviewed.
Teks lengkap: Headnote
Hypertension affects 10% of pregnancies in the United States and remains a leading cause of both maternal
and fetal morbidity and mortality. Hypertension in pregnancy includes a spectrum of conditions, most notably
preeclampsia, a form of hypertension unique to pregnancy that occurs de novo or superimposed on chronic
hypertension. Risks to the fetus include premature delivery, growth retardation, and death. The only definitive
treatment of preeclampsia is delivery. Treatment of severe hypertension is necessary to prevent
cerebrovascular, cardiac, and renal complications in the mother. The 2 other forms of hypertension, chronic and
transient hypertension, usually have more benign courses. Optimal treatment of high blood pressure in
pregnancy requires consideration of several aspects unique to gestational cardiovascular physiology. The major
goal is to prevent maternal complications without compromising uteroplacental perfusion and fetal circulation.
Before an antihypertensive agent is prescribed, the potential risk to the fetus from intrauterine drug exposure
should be carefully reviewed.
Mayo Clin Proc. 2000;75:1071-1076
ACE = angiotensin-converting enzyme; DBP = diastolic blood pressure; HELLP = hemolysis, elevated liver
enzymes, low platelet count; NHBPEP = National High Blood Pressure Education Program; SBP = systolic
blood pressure
Normal pregnancy is characterized by increases in cardiac output and blood volume, generalized
vasodilatation, a decrease in blood pressure, and resistance to pressor agents such as norepinephrine and
angiotensin 11.1 Blood pressure achieves a nadir by midpregnancy, then returns to prepregnancy levels at
term. Systolic blood pressure (SBP) is less affected than diastolic blood pressure (DBP) because of the
increased cardiac output that offsets the vasodilatation. Further decline is noted during sleep, which follows the
pattern of normal circadian rhythms observed in nonpregnant women.
DEFINITION AND CLASSIFICATION
Hypertension in pregnancy is defined as a blood pressure of 140/90 mm Hg or higher. Korotkoff phase V
(disappearance) rather than Korotkoff phase IV (muffling of sounds) is used for the determination of DBP.2 In
the outpatient setting, blood pressure should be measured in the sitting position, after a period of rest in a quiet
environment. For hospitalized patients, the lateral recumbent position eliminates the effect of compression of
the inferior vena cava by the enlarged uterus that impairs venous return and causes a decline in blood pressure.
Regardless of posture, special care should be taken to ensure that the patient's arms are kept at the heart level;
positioning the arms above the heart can spuriously reduce the blood pressure readings. In pregnancy, the
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lowest blood pressures are obtained by using the right arm while the patient is resting in the left lateral
position.3 These blood pressure readings might merely reflect the changes in hydrostatic pressure caused by
keeping the right arm above the heart. Therefore, the increases in blood pressure with a change from a lateral
to a supine position may simply represent a postural phenomenon rather than positive results on a rollover test,
once considered a predictor of preeclampsia.4
The Working Group of the National High Blood Pressure Education Program (NHBPEP) recently published a
second report revising the classification of hypertensive disorders in pregnancy.2 The term transient
hypertension was replaced by gestational hypertension, which is used only during pregnancy for a group of
women who develop high blood pressure for the first time after 20 weeks' gestation in the absence of
proteinuria. The rest of the classification remains unchanged (Table 1).
Preeclampsia
Preeclampsia is a multisystemic disease characterized by hypertension and proteinuria, a protein level of 300
mg or greater in a 24-hour urine specimen that roughly correlates with a qualitative measurement of 1+ (30
mg/dL) on dipstick urinalysis in the absence of urinary tract infection. Because of disagreement between
random and 24-hour urinary protein determinations, the latter is recommended for diagnostic purposes. If this is
not feasible, a timed urinary collection corrected for creatinine excretion is an acceptable alternative. The
diagnosis of hypertension is supported by recording elevated blood pressure on 2 determinations performed 6
hours apart.
An important feature of preeclampsia is its unpredictable clinical course; women with mild hypertension And
minimal proteinuria can have rapid progression to the convulsive form of eclampsia. Thus, distinguishing
between "mild" and "severe" forms is discouraged because it can be clinically misleading.5 However, certain
symptoms and signs are considered markers of severe disease and necessitate close monitoring and,
frequently, urgent delivery. These include an SBP of 160 mm Hg or higher and a DBP of 110 mm Hg or higher,
nephrotic range proteinuria (protein level >3.5 g/24 h), renal functional impairment (serum creatinine level >1.2
mg/dL), thrombocytopenia (platelet count <100 x 10^sup 9^/L), and/or evidence of microangiopathic hemolytic
anemia, hepatocellular injury, pulmonary edema, and neurologic disturbances.
Preeclampsia usually occurs after 20 weeks of gestation and traditionally is considered a disease of the first
pregnancy. However, women with a history of preeclampsia have an increased risk during subsequent
pregnancies. Other risk factors include extremes of reproductive age, multiple gestations (eg, twins), family
history of preeclampsia, and the presence of trophoblastic disease, chronic hypertension, diabetes mellitus,
connective tissue disease, and renal disease. The hemodynamic changes include decreased cardiac output
relative to normal pregnancy, elevated peripheral vascular resistance,6 and loss or reversal of the normal
diurnal rhythm, resulting in elevated nocturnal blood pressure readings.
The hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome is a deceptive form of
preeclampsia. It can rapidly evolve into a life-threatening syndrome of liver failure and worsening
thrombocytopenia in the presence of only mild to moderate hypertension. The most severe complication of the
HELLP syndrome is liver rupture, which has high maternal and fetal mortality rates.
The cause and pathogenesis of preeclampsia remain elusive. Consequently, specific preventive and treatment
options have not been developed. Ideally, high-risk patients should be evaluated early in pregnancy by an
obstetrician with special expertise in this field. The baseline values for hemoglobin, hematocrit, platelet count,
serum uric acid, creatinine, and protein excretion should be obtained because a comparison with values later in
pregnancy may help in establishing the diagnosis of preeclampsia.
Patients presenting with hypertension in the second half of pregnancy should be additionally monitored for
hepatic involvement (serum transaminase levels), presence of hemolysis (lactic acid dehydrogenase level and
blood smear), and degree of capillary leak (serum albumin level). These tests are particularly useful in
monitoring disease severity and progression.2
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If preeclampsia develops at less than 32 weeks' gestation, when the fetus is still immature, consideration should
be given to postponing delivery.7 This is a reasonable approach when hypertension is mild, and no renal, liver,
or coagulation abnormalities are evident. Patients should be hospitalized and closely monitored for signs of fetal
distress and symptoms of headache, visual disturbances, and right upper quadrant pain that may herald
progression to more severe forms, including eclampsia. The threshold for initiation of antihypertensive therapy
is the same as for severe preeclampsia, ie, DBP of 100 mm Hg or higher. An oral agent is preferred if delivery is
not expected within 48 hours.5 Outpatient management can be considered for asymptomatic patients with
treatment-responsive hypertension in the absence of marked proteinuria (protein level <1 g/24 h).
Labor should be induced when pregnancies are at or near term and in women with severe hypertension
persisting after 24 to 48 hours of treatment, HELLP syndrome, progressive renal failure, premonitory signs of
eclampsia, and fetal distress.8 Patients having severe preeclampsia at less than 34 weeks' gestation should
receive corticosteroids to accelerate fetal lung development. Intravenous magnesium sulfate therapy has been
shown to be more effective than either phenytoin or diazepam for seizure prophylaxis in women with severe
preeclampsia and for prevention of recurrent seizures in those with eclampsia. Magnesium sulfate should be
administered during labor and delivery and for at least 24 hours postpartum by continuous intravenous infusion.
To avoid magnesium toxicity in women with renal insufficiency, the maintenance dose should be reduced, and
the serum magnesium levels should be monitored every 1 to 2 hours (compared to every 4-6 hours in women
with normal renal function) until a steady state is reached. Effective therapy for magnesium toxicity is
intravenous calcium gluconate, which should be available at the bedside.
Studies have shown that pharmacological treatment of DBP of 110 mm Hg or greater decreases the incidence
of acute maternal cardiac and cerebral insults.9 Most investigators agree that antihypertensive therapy in the
peripartum period should be initiated when the DBP approaches 100 mm Hg.5 The most important reason for
treatment of hypertension is the prevention of maternal cerebrovasular and cardiac complications. Control of
blood pressure does not prevent or cure preeclampsia. In fact, eclamptic seizures can occur when the blood
pressure is only mildly elevated.
Chronic Hypertension
The hallmark of chronic hypertension is a blood pressure of 140/90 mm Hg or greater before pregnancy or
before the 20th week of gestation. Most patients will have a benign course with an exaggerated decrease in
DBP of as much as 20 mm Hg. This often leads to normalization of blood pressure in midpregnancy10 and may
mask the diagnosis of chronic hypertension if prepregnancy values are unknown. The blood pressure usually
increases to prepregnancy levels in the third trimester, frequently leading to diagnostic confusion with
preeclampsia. Proteinuria is absent in uncomplicated chronic hypertension, and when it occurs for the first time
in the third trimester, it is the best indicator of superimposed preeclampsia. Antihypertensive treatment is usually
instituted for an SBP of 150 mm Hg or greater or a DBP of 100 mm Hg or greater, unless there is evidence of
renal disease or other target organ complications.' In these instances, antihypertensive therapy is initiated when
the DBP is 90 mm Hg or greater. Women with chronic hypertension are at an increased risk for developing
preeclampsia, particularly if the blood pressure does not decline in midgestation or if they have secondary
hypertension. Ideally, they should be evaluated before pregnancy for end-organ damage, such as left
ventricular hypertrophy, hypertensive nephropathy, and retinopathy. A work-up of secondary hypertension
should be considered (eg, primary hyperaldosteronism, renovascular disease, pheochromocytoma), particularly
in young patients with hard-to-control blood pressure requiring several antihypertensive agents. Medications
prescribed before pregnancy can be continued during pregnancy except for angiotensinconverting enzyme
(ACE) inhibitors and angiotensin II receptor blockers. Women taking these medications who present for
prepregnancy counseling should be told to use another agent (eg, methyldopa) before conception.
The combination of hypertension and kidney disease is associated with increased risks of fetal loss,
prematurity, and intrauterine growth retardation. Women with chronic renal diseases should be advised to plan
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their pregnancies while their renal function is relatively preserved (serum creatinine level <1.4 mg/dL)2 because
fetal prognosis has improved with the neonatal care currently available. Such patients require the collaborative
efforts of a multidisciplinary team, including high-risk obstetrics, nephrology, and hypertension, for optimal
treatment.
Women with preeclampsia superimposed on chronic hypertension are at a particularly high risk for cerebral
hemorrhage and placental abruption. It remains unclear whether early treatment of chronic hypertension in
pregnancy prevents preeclampsia. Several randomized trials have failed to demonstrate that treatment of
chronic hypertension reduces the incidence of superimposed preeclampsia.11 The main criticism of these trials
was inadequate sample size; moreover, only 1 trial12 was placebocontrolled. The continued uncertainty can be
resolved only by carefully designed clinical trials, which are urgently needed.
Gestational Hypertension
Gestational hypertension is characterized by hypertension occurring for the first time in the second half of
pregnancy in the absence of proteinuria. This category encompasses both women with preeclampsia who have
not yet developed proteinuria and those with hypertension only. The differentiation between these 2 groups is
possible only retrospectively, ie, postpartum. Transient hypertension (the term previously used for this category)
refers to a subgroup of women in whom blood pressure returns to normal by 12 weeks' postpartum. The failure
of blood pressure to normalize leads to the diagnosis of chronic hypertension. Transient hypertension has a
benign course and good prognosis, with a tendency to recur in subsequent pregnancies. The blood pressure
usually normalizes shortly after delivery, although the risk of developing hypertension later in life is increased.13
TREATMENT
Goals for the treatment of hypertension in pregnancy differ from those for the general hypertensive population.
The benefit of treatment of mild diastolic hypertension, blood pressure of 90 to 99 mm Hg, has been clearly
established and documented for the general population, while in pregnancy it remains an area of controversy in
the absence of well-designed clinical trials.
The choice of antihypertensive medication in pregnancy is limited by concerns for fetal safety. In addition to
proven safety, an ideal antihypertensive agent should gradually reduce blood pressure without compromising
uteroplacental blood flow to the fetus. If administered intravenously, a short-acting formulation that permits rapid
reversal of hypotension is preferred. According to the Working Group report of the NHBPEP,2 first-line oral and
intravenous treatment is methyldopa and hydralazine, respectively. Methyldopa is the only antihypertensive
agent with a proven record of safety in pregnancy, established by follow-up studies of children exposed to the
drug in utero.14 Because of its long history of efficacy and acceptable sideeffect profile, intravenous hydralazine
is recommended for the treatment of severe hypertension in women who are near term. Other antihypertensive
medications are now being used more often, particularly if blood pressure control cannot be achieved with firstline agents or in the presence of intolerable adverse effects. Some of the newer agents have demonstrated
efficacy and safety comparable to those of methyldopa and hydralazine.
(beta)-Blockers have demonstrated effective blood pressure control and a satisfactory safety profile when
administered in the third trimester. Labetalol has been used with increasing frequency for the treatment of
severe acute hypertension during pregnancy and has shown efficacy and tolerance equivalent to hydralazine.15
The main concerns about the use of beta-blockers stem from evidence of intrauterine growth retardation and
low placental weight documented when atenolol was used in the second trimester.16 betaBlockers can
potentially cause additional adverse effects, such as fetal bradycardia, impaired fetal compensatory response to
hypoxia, and neonatal hypoglycemia.
Data on the safety and efficacy of calcium channel blockers, especially early in pregnancy, are limited. Calcium
channel blockers are potent tocolytics and can affect the progression of labor. Another concern is the potential
for profound hypotension and circulatory collapse when magnesium sulfate is used concurrently with calcium
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channel blockers for seizure prophylaxis. In pregnancy, calcium channel blockers are increasingly used for
severe hypertension refractory to other drugs. Nifedipine has been studied most extensively and has been
shown to decrease blood pressure and improve renal function without affecting blood flow in the umbilical
artery. 17 As in other settings, the availability of long-acting preparations has mitigated the risk of precipitous
blood pressure decreases that can potentially compromise uteroplacental blood flow and fetal well-being.
According to the Working Group report of the NHBPEP, diuretics can be continued during pregnancy if initiated
before conception, especially in women with salt-sensitive chronic hypertension.2 Other indications for diuretic
therapy are hypertension in the setting of renal failure and congestive heart failure. Possible adverse effects
include electrolyte abnormalities such as hyponatremia, hypokalemia, and hyperuricemia. Diuretics can
aggravate volume depletion and promote reactive vasoconstriction and should be avoided in women with
preeclampsia.
ACE inhibitors are contraindicated in pregnancy. They adversely affect the fetal renal system, causing anuria
and oligohydramnios. Complications reported in newborns after in utero exposure during the second and third
trimester include fetal limb abnormalities, lung hypoplasia, craniofacial deformities, and renal dysplasia.18
Angiotensin II receptor blockers exert a similar hemodynamic effect on fetal renal circulation and can potentially
cause similar fetal malformations. Fetuses of women who take ACE inhibitors or angiotensin II receptor blockers
during the first trimester are not considered at a higher risk for these malformations, and women exposed to
such agents during this time do not need to terminate their pregnancy.
Finally, direct vasodilators, other than hydralazine, may need to be considered for the rare patient with severe
refractory hypertension. Direct vasodilators can cause severe complications, such as excessive hypotension
(both sodium nitroprusside and diazoxide) and cyanide intoxication (sodium nitroprusside only), making them
the agents of last resort."
Nonpharmacological treatment consists mainly of bed rest, which has been shown not only to lower blood
pressure but also to promote diuresis and reduce premature labor.19 However, pregnant women with sodiumsensitive chronic hypertension should continue salt restriction during pregnancy. Salt restriction is not
recommended for routine treatment of women with preeclampsia, who frequently are volume contracted.
Prevention of preeclampsia has been attempted by using several strategies. Some have proved to be
unsuccessful, such as salt restriction,20 magnesium,21 and fish oil supplementation22; others are potentially
dangerous (diuretics). The role of low-dose aspirin has been studied in several large trials, including the
multicenter Collaborative Lowdose Aspirin Study in Pregnancy (CLASP)23 trial that failed to show a beneficial
effect of aspirin in the prevention of preeclampsia. Although the study was designed to include women with a
higher risk, the incidence of preeclampsia in the placebo group was only 7.6%, similar to that in the general
population. Therefore, the issue of the role of aspirin in high-risk groups remained unclear. In 1998, the National
Institutes of Health published the results of a double-blind, randomized, placebo-controlled trial of the role of
low-dose aspirin in the prevention of preeclampsia in 2539 women at higher risk (history of chronic
hypertension, insulin-treated diabetes mellitus, multifetal gestations, and preeclampsia in previous
pregnancy).24 The demonstrated benefit was too small to justify routine prophylaxis: 38 women would need to
be treated to prevent 1 case of preeclampsia. Similarly, low-dose aspirin did not improve perinatal outcomes in
these women. Calcium supplementation, beyond the daily recommended level, also proved of no benefit in a
large National Institutes of Health trial of 4589 healthy nulliparous women. 25 The potential benefit of
antioxidants, vitamins C and E, was recently investigated in women at increased risk.26 When initiated at 16 to
22 weeks' gestation at doses of 1000 mg and 400 IU daily, respectively, a reduction in plasma markers of
endothelial injury and a decreased incidence were observed in the treated group compared with the placebo
group. While the investigators recognized the need for multicenter trials to assess the effects in low-risk and
high-risk patients from different populations, these studies should also address the issues of safety, particularly
for the fetus, of vitamins C and E at the recommended doses.
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CONCLUSION
The ultimate goal of treatment of hypertension in pregnancy is delivery of a healthy newborn without
compromising maternal health. Early diagnosis and subsequent close monitoring of both mother and fetus are
crucial. Elevated blood pressure without proteinuria usually has a benign course and can be managed on an
outpatient basis. Antihypertensive medications should be used judiciously, and fetal risks from intrauterine
exposure must be carefully evaluated. Severe preeclampsia (both pure and superimposed) represents an
obstetrical emergency, with potential fatal outcomes for both fetus and mother. Optimally, such women should
be hospitalized and treated with bed rest, antihypertensive medications, and magnesium sulfate for seizure
prophylaxis. The definitive treatment of preeclampsia is delivery. For mild forms remote from term, postponing
delivery is desirable and, if possible, can improve neonatal prognosis by decreasing prematurity.
Questions About Hypertension in Pregnancy
1. Which one of the following can help distinguish superimposed preeclampsia from chronic hypertension?
a. Severe hypertension with blood pressure greater than 180/100 mm Hg
b. Onset of proteinuria in the third trimester
c. Onset of hypertension in the third trimester
d. Normal renal function
e. Edema
2. Which one of the following is correct concerning
ACE inhibitors in pregnancy?
a. They are contraindicated
b. They are always an indication for therapeutic abortion
c. They should be replaced by angiotensin II receptor blockers
d. They have peak teratogenic potential during the first trimester
e. They are less harmful later in pregnancy
3. Which one of the following antihypertensive drugs has been proved to be safe in pregnancy based on followup studies of children exposed in utero?
a. Nifedipine
b. Hydralazine
c. Methyldopa
d. Labetalol
e. Hydrochlorothiazide
4. Which one of the following is the most effective agent for the prevention of eclamptic seizures?
a. Methyldopa
b. Phenytoin
c. Diazepam
d. Magnesium sulfate
e. Calcium gluconate
5. A 32-year-old multigravida presents with increasing leg edema at 34 weeks' gestation. Physical examination
findings are unremarkable except for 2+ pretibial edema and a blood pressure of 155/95 mm Hg. The serum
creatinine level, uric acid value, liver function test results, and findings on dipstick urinalysis are normal. During
a pregnancy 4 years ago, she had an elevated blood pressure that quickly normalized after spontaneous
vaginal delivery. She has taken no antihypertensive drugs. Which one of the following is the most likely
diagnosis?
a. Recurrent "pure" preeclampsia
b. Preeclampsia superimposed on chronic hypertension
c. Chronic hypertension
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d. Gestational hypertension
e. Normal pregnancy Correct answers:
1. b, 2. a, 3. c, 4. d, 5. d
Sidebar
Table 1. Classification of Hypertensive Disorders in Pregnancy2
Preeclampsia-eclampsia
Preeclampsia superimposed on chronic hypertension
Chronic hypertension
Gestational hypertension
References
REFERENCES
1. McLaughlin MK, Roberts JM. Hemodynamic changes. In:
Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley's Hypertensive Disorders in Pregnancy. 2nd ed.
Stamford, Conn: Appleton &Lange; 1999:69-102.
2. National High Blood Pressure Education Program Working Group Report on High Blood Pressure in
Pregnancy. Report of the National High Blood Pressure Education Program Working Group on High Blood
Pressure in Pregnancy. Am J Obstet Gynecol. 2000; 183(l, suppl):51-522.
3. Van Dongen PW, Eskes TK, Martin CB, Van 't Hof MA. Postural blood pressure differences in pregnancy: a
prospective study of blood pressure differences between supine and left lateral position as measured by
ultrasound. Am J Obstet GynecoL 1980;138:15.
References
4. Lindheimer MD, Roberts JM, Cunningham FG, Chesley L. Introduction, history, controversies, and definitions.
In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley's Hypertensive Disorders in Pregnancy. 2nd ed.
Stamford, Conn: Appleton &Lange; 1999:3-41.
5. August P. Preeclampsia: new thoughts on an ancient problem. J Clin Hypertens. 2000;2:115-123.
6. Visser W, Wallenburg HC. Central hemodynamic observations in untreated preeclamptic patients.
Hypertension. 1991;17:10721077.
References
7. Sibai BM, Mercer BM, Schiff E, Friedman SA. Aggressive versus expectant management of severe
preeclampsia at 28 to 32 weeks' gestation: a randomized controlled trial. Am J Obstet GynecoL 1994;171:818822.
8. Cunningham FG, Lindheimer MD. Hypertension in pregnancy. N Engl J Med. 1992;326:927-932.
9. Sibai BM, Anderson GD. Pregnancy outcome of intensive therapy in severe hypertension in first trimester.
Obstet GynecoL 1986;67: 517-522.
References
10. Sibai BM, Abdella TN, Anderson GD. Pregnancy outcome in 211 patients with mild chronic hypertension.
Obstet GynecoL 1983;61: 571-576.
11. Sibai BM. Treatment of hypertension in pregnant women. NEngl J Med. 1996;335:257-265.
12. Weitz C, Khouzam V, Maxwell K, Johnson JW. Treatment of hypertension in pregnancy with methyldopa: a
randomized double blind study. Int J Gynaecol Obstet. 1987;25:35-40.
13. Chesley LC, Sibai BM. Clinical significance of elevated mean arterial pressure in the second trimester. Am J
Obstet Gynecol. 1988;159:275-279.
14. Cockburn J, Moar VA, Ounsted M, Redman CW. Final report of study on hypertension during pregnancy:
the effects of specific treatment on the growth and development of the children. Lancet. 1982;1:647-649.
15. Umans JG, Lindheimer MD. Anti hypertensive treatment. In: Lindheimer MD, Roberts JM, Cunningham FG,
eds. Chesley's Hypertensive Disorders in Pregnancy. 2nd ed. Stamford, Conn: Appleton &Lange; 1999:58123 February 2015

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604.
16. Butters L, Kennedy S, Rubin PC. Atenolol in essential hypertension during pregnancy. BMJ. 1990;301:587589.
17. Ismail AA, Medhat I, Tawfic TA, Kholeif A. Evaluation of calcium-antagonist (Nifedipine) in the treatment of
pre-eclampsia. Int J Gynaecol Obstet. 1993;40:39-43.
18. Pryde PG, Sedman AB, Nugent CE, Barr M Jr. Angiotensin-converting enzyme inhibitor fetopathy. J Am Soc
Nephrol. 1993;3: 1575-1582.
References
19. Papiernik E, Kaminski M. Multifactorial study of the risk of prematurity at 32 weeks of gestation, I: a study of
the frequency of 30 predictive characteristics. J Perinat Med. 1974;2:30-36.
20. Steegers EA, Eskes TK, Jongsma HW, Hein PR. Dietary sodium restriction during pregnancy: a historical
review. Eur J Obstet Gynecol Reprod Biol. 1991;40:83-90.
21. Spading L, Spading G. Magnesium supplementation in pregnancy: a double-blind study. BrJ Obstet
Gynaecol. 1988;95:120-125.
22. Salvig JD, Olsen SF, Secher NJ. Effects of fish oil supplementation in late pregnancy on blood pressure: a
randomised controlled trial. Br J Obstet Gynaecol. 1996;103:529-533.
23. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomised
trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women.
Lancet. 1994;343:619-629.
24. Caritis S, Sibai B, Hauth J, et al. Low-dose aspirin to prevent preeclampsia in women at high risk. N Engl
JMed. 1998;338:701-705. 25. Levine RJ, Hauth JC, Curet LB, et al, National Institute of Child
Health and Human Development Network of Maternal-Fetal Medicine Units. Trial of calcium to prevent
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AuthorAffiliation
VESNA D. GAROVIC, MD
AuthorAffiliation
From the Divisions of Hypertension and Nephrology, Department of Internal Medicine, and Pregnancy-Related
Hypertension and Kidney Disease Clinic, Mayo Clinic, Rochester, Minn.
Address reprint requests and correspondence to Vesna D. Garovic, MD, Division of Hypertension, Mayo Clinic,
200 First St SW, Rochester, MN 55905.
MeSH: Antihypertensive Agents -- therapeutic use, Chronic Disease, Female, Fetal Viability -- physiology,
Humans, Hypertension -- drug therapy, Hypertension -- physiopathology, Maternal-Fetal Exchange, Placental
Circulation -- physiology, Pre-Eclampsia -- diagnosis, Pre-Eclampsia -- drug therapy, Pregnancy, Pregnancy
Complications, Cardiovascular -- drug therapy, Pregnancy Complications, Cardiovascular -- physiopathology,
Risk Factors, Hypertension -- diagnosis (utama), Pregnancy Complications, Cardiovascular -- diagnosis (utama)
Substansi: Antihypertensive Agents;
Judul: Hypertension in pregnancy: Diagnosis and treatment
Pengarang: Garovic, Vesna D
Judul publikasi: Mayo Clinic Proceedings
Volume: 75
Edisi: 10

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Halaman: 1071-6
Jumlah halaman: 6
Tahun publikasi: 2000
Tanggal publikasi: Oct 2000
Tahun: 2000
Penerbit: Mayo Foundation for Medical Education and Research
Tempat publikasi: Rochester
Negara publikasi: United States
Subjek publikasi: Medical Sciences
ISSN: 00256196
CODEN: MACPAJ
Jenis sumber: Scholarly Journals
Bahasa publikasi: English
Jenis dokumen: Journal Article
Nomor aksesi: 11040855
ID dokumen ProQuest: 216873268
URL Dokumen: http://search.proquest.com/docview/216873268?accountid=25704
Hak cipta: Copyright Mayo Foundation for Medical Education and Research Oct 2000
Terakhir diperbarui: 2014-01-15
Basis data: ProQuest Public Health

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