Published online before print February 7, 2008, doi: 10.1161/HYPERTENSIONAHA.107.104646
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(Hypertension. 2008;51:1027.)
© 2008 American Heart Association, Inc.
Go Red Original Articles |
Mean Arterial Pressure at 11+0 to 13+6 Weeks in the Prediction of Preeclampsia
From the Harris Birthright Research Centre for Fetal Medicine, King’s College Hospital, London, United Kingdom.
Correspondence to Nikos A. Kametas, Harris Birthright Research Centre for Fetal Medicine, King’s College Hospital, Denmark Hill, London SE5 9RS, United Kingdom. E-mail n.kametas{at}btinternet.com
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Abstract |
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This study aimed to determine the performance of screening for preeclampsia (PE) by maternal medical history and mean arterial pressure (MAP) at 11+0 to 13+6 weeks. In 5590 women with singleton pregnancies attending for routine care at 11+0 to 13+6 week’s gestation we recorded maternal variables and measured the MAP. We excluded 397 because they had missing outcome data or the pregnancies resulted in miscarriage or termination. In 104 patients there was subsequent development of PE, 97 developed gestational hypertension, 574 delivered small-for-gestational-age newborns, and 4418 were unaffected by PE, gestational hypertension, or small for gestational age. A multivariate Gaussian model was fitted to the distribution of log multiple of the median MAP in the PE and unaffected groups. Likelihood ratios for log multiple of the median MAP were computed and used together with maternal variables to produce patient-specific risks for each case. Detection rates and false-positive rates were calculated by taking the proportions with risks above a given risk threshold. In the unaffected group, log MAP was influenced by maternal age, ethnic origin, smoking, family and personal history of PE, and fetal crown-rump length. In the prediction of PE, significant contributions were provided by log multiple of the median MAP, ethnic origin, body mass index, and personal history of PE. The detection rate of PE by log multiple of the median MAP and maternal variables was 62.5% for a false-positive rate of 10%. Maternal variables, together with MAP, at 11+0 to 13+6 weeks identify a group at high risk for development of PE.
Key Words: first trimester • mean arterial pressure • pregnancy • preeclampsia • screening
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Introduction |
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Preeclampsia (PE), which affects
2% of pregnancies, is a major cause of perinatal and maternal morbidity and mortality.1–3 Attempts at prevention of PE by prophylactic interventions from midgestation have been largely unsuccessful.4–7 It is uncertain whether interventions starting from the first rather than the second trimester would prove to be more effective in the prevention of PE, but before this could be investigated, it is essential to develop a method of effective and early identification of the high-risk group.
The likelihood of developing PE is increased by a number of factors in the maternal history, including Afro-Caribbean ethnicity, nulliparity, high body mass index (BMI), and previous or family history of PE.8,9 However, screening by maternal history alone will detect only 30% of those who will develop PE, for a false-positive rate (FPR) of 10%.9
The diagnosis of PE is based on the demonstration of high blood pressure (BP) and significant proteinuria during the second half of pregnancy in previously normotensive women. Several second-trimester studies have reported on the use of BP measurement as a screening method for subsequent development of PE. These studies have reported contradictory results with FPR ranging from 7% to 52% and detection rates (DRs) ranging from 8% to 93% (Table 1).10–19 These differences are likely to be the consequence of the varied methods in selection of the screened population, measurement of BP, cutoffs used in defining the screen-positive group, and definitions of PE. There are 2 first-trimester screening studies for PE. The first study used an automated device to measure BP in 983 women at 9 to 12 weeks and reported that, with a cutoff of 90 mm Hg in mean arterial pressure (MAP), the DR of PE was 62%, for an FPR of 38%.15 However, the definition of PE used in this study is not accepted by any professional organization, because it was based on the development of gestational hypertension (GH) with either weight gain or a reading of only 1+ of protein on dipstick analysis on 1 occasion. The second study was a retrospective one in which the medical charts of pregnant women attending for routine prenatal care were examined to identify the BP measurements taken by mercury sphygmomanometers before 20 weeks (mean: 13.7 weeks) from 1655 women.20 At a cutoff of 92 mm Hg in MAP, the DR of PE was 25%, for an FPR of 10%.
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In current clinical practice, the use of mercury sphygmomanometers remains the gold standard for noninvasive BP monitoring, but there are concerns for both the clinical performance and safety of these instruments.21,22 These problems have been largely overcome by the use of automated BP devices, but so far only 1 of these has been validated for use both in pregnancy and in PE.23
We used a validated automated device to prospectively measure the MAP at 11+0 to 13+6 weeks in 5590 singleton pregnancies attending for routine pregnancy care.23 The aim of our study was to determine the performance of screening for PE by maternal characteristics and measurement of MAP at 11+0 to 13+6 weeks.
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Methods |
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This was a prospective screening study for PE in singleton pregnancies. All of the women were attending our center for routine assessment of risk for chromosomal abnormalities by measurement of fetal nuchal translucency thickness and maternal serum-free β-human chorionic gonadotropin and pregnancy-associated plasma protein A at 11+0 to 13+6 weeks of gestation between March and December 2006.24,25 Gestational age was derived from the fetal crown-rump length (CRL). Written informed consent was obtained from the women agreeing to participate in the study, which was approved by King’s College Hospital Ethics Committee.
Patients were asked to complete a questionnaire on maternal age, ethnic origin (white, Afro-Caribbean, Indian or Pakistani, Chinese or Japanese, or mixed), cigarette smoking during pregnancy (yes or no), alcohol intake during pregnancy (yes or no), drug abuse during pregnancy (yes or no), medical history (including chronic hypertension, diabetes mellitus, antiphospholipid syndrome, thrombophilia, HIV infection, and sickle cell disease), medication (including antihypertensive, antidepressant, antiepileptic, anti-inflammatory, antiretroviral, antithyroid, aspirin, betamimetic, insulin, lithium, steroids, or thyroxin), parity (parous or nulliparous if no delivery beyond 23 weeks), obstetric history (including previous pregnancy with PE), and family history of PE (sister, mother, or both). The maternal weight and height were measured, and the BMI was calculated in kilograms per meter squared.
The BP was taken by automated devices (3BTO-A2, Microlife), which were calibrated before and at regular intervals during the study. The recordings were made by doctors who had received appropriate training on the use of these machines. The women were in the seated position, their arms were supported at the level of the heart, and a small (<22-cm), normal (22- to 32-cm), or large (33- to 42-cm) adult cuff was used depending on the midarm circumference.26 After rest for 5 minutes, BP was measured in both arms simultaneously, and a series of recordings were made at 1-minute intervals until variations between consecutive readings fell within 10 mm Hg in systolic and 6 mm Hg in diastolic BP in both arms.27 When this point of stability was reached, we calculated the MAP of each arm as the average of the last 2 stable measurements, and, as recommended, we took the arm with the highest final MAP for the subsequent analysis of results.27
The MAP, ultrasound findings, and woman’s characteristics, including demographic data and obstetric and medical history, were entered into a computer database. Data on pregnancy outcome were collected from the hospital maternity records or their general medical practitioners. The obstetric records of all of the women with pre-existing or pregnancy associated hypertension were examined to determine whether the condition was chronic hypertension, PE, or GH. Similarly, for quality control, we examined the records of 500 randomly selected patients without pregnancy-associated hypertension.
Outcome Measures
The outcome measures were PE and GH with or without small for gestational age. The group of patients with PE included those with PE superimposed on chronic hypertension.
The definitions of PE and GH were those of the International Society for the Study of Hypertension in Pregnancy.28 In patients with GH, the diastolic BP should be 
90 mm Hg on 2 occasions 4 hours apart developing after 20 weeks of gestation in previously normotensive women in the absence of significant proteinuria, and in patients with PE there should be GH with proteinuria of 300 mg in 24 hours or 2 readings of at least ++ on dipstick analysis of midstream or catheter urine specimens if no 24-hour collection is available. In chronic hypertension there should be a history of hypertension before conception or the presence of hypertension at the booking visit before 20 weeks of gestation in the absence of trophoblastic disease. In PE superimposed on chronic hypertension, significant proteinuria (as defined above) should develop after 20 weeks of gestation in women with known chronic hypertension.28
Statistical Analysis
The following 8 steps were taken. First, the women were subdivided into 3 groups depending on pregnancy outcome: PE, GH, and unaffected by PE or GH and delivering babies with birth weight above the 10th percentile after correction for gestation at delivery and sex of the newborn, maternal ethnic origin, weight, height, and parity.29 Second, the distribution of MAP was made Gaussian after logarithmic transformation. Third, multiple regression analysis was used to determine which of the factors among the maternal characteristics, medical and obstetric history, and gestation (see Table 2) were significant predictors of log MAP in the unaffected group. Fourth, the distribution of log MAP, expressed as multiples of the median (MoMs) of the unaffected group, was determined in the PE and GH groups. Fifth, multiple regression analysis was used to determine which of the factors among the maternal characteristics, medical and obstetric history and gestation (see Table 2), had a significant contribution in explaining the a priori risk for PE and GH. Sixth, likelihood ratios were computed from the fitted distributions of log MoM values in the unaffected pregnancies and in each of the 2 groups with pregnancy complications. Seventh, patient-specific risks for each complication were derived by multiplying the appropriate a priori risk with the likelihood ratio. Eighth, the DR and FPR were calculated as the respective proportions of PE and GH (DR) and unaffected pregnancies (FPR) with MoM values above given cutoffs. The statistical software package SPSS 15.0 (SPSS Inc) was used for all of the data analyses.
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Results |
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Study Population
First-trimester screening was carried out in 5590 consecutive singleton pregnancies with a live fetus at 11+0 to 13+6 weeks. We excluded 397 (7.1%) because they had missing outcome data (n=289), the pregnancies resulted in fetal death or miscarriage before 24 weeks of gestation (n=50), or the pregnancies were terminated for fetal abnormalities (n=49) or social reasons (n=9). In the remaining 5193 subjects there were 104 (2.0%) who developed PE, including 6 subjects with PE superimposed on chronic hypertension, 97 (1.9%) who developed GH, 574 (11.0%) who did not develop PE or GH but delivered small-for-gestational-age newborns, and 4418 (85.1%) subjects who were unaffected by PE, GH, or small for gestational age. In the quality control assessment of the 500 subjects with reported normal outcome, there was 1 subject with GH. The characteristics of the 3 outcome groups are summarized in Table 2.
The difference in BP between the first 2 measurements was <10 mm Hg for the systolic BP and <6 mm Hg for the diastolic BP in 4524 subjects (87.1%). It became necessary to have 3 recordings (10.1%) in 525, 4 (1.7%) in 89, 5 (0.7%) in 36, and 6 or 7 (0.4%) in 19.
Log MAP in the Unaffected Group
In the multiple regression model for log MAP, significant independent contributions were provided by maternal ethnic origin, age, BMI, previous history of PE, maternal history of PE, cigarette smoking, and fetal CRL.
Log MAP=1.8666–0.0002xCRL (in mm)+(–0.0035 if Afro-Caribbean, –0.0075 if Indian or Pakistani, –0.0132 if Chinese or Japanese, –0.0077 if mixed, or 0 if white)+ 0.0005xage (in years)+0.0024xBMI (in kg/m2)+(0.0057 if woman’s mother had PE or 0 if she did not)+(–0.008 if parous without previous PE, 0.009 if parous with previous PE or 0 if nulliparous)+(–0.0078 if smoker or 0 if not smoker; R2=0.120; P<0.001).
Distributions of log MoM MAP
In each woman we, first, logarithmic transformed the measured MAP (log-observed MAP), second, used the formula above for log MAP in the unaffected group to calculate the log expected MAP, and, third, calculated the ratio of the observed-to-expected values: log (observed/expected)=log MoM MAP=log observed–log expected.
The mean (95% CI of the mean) MoM MAP was 1.0 (1.0008 to 1.0055) MoM in the unaffected group, 1.0840 (1.0649 to 1.1032) MoM in the PE group, and 1.0646 (1.0452 to 1.0839) MoM in the GH group (Figure 1). Therefore, the mean MoM MAP in both the PE and GH groups was significantly higher than in the unaffected group. The mean MoM MAP did not change significantly with gestation at delivery in either the PE (r=0.184; P=0.059) or the GH group (r=0.155; P=0.130).
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Likelihood Ratios for PE and GH
The overlapping Gaussian distributions of log MoM MAP in the unaffected group and each of the PE and GH groups were used to calculate the likelihood ratios for each pregnancy complication (Table 3).
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The A Priori Risk for PE and GH
The a priori risk for each pregnancy complication is calculated from the following formula: odds/(1+odds), where odds=eY and Y is derived from multiple regression analysis of maternal characteristics, medical and obstetric history. For PE: Y=–6.311+(1.299 if Afro-Caribbean or 0 if other ethnic origin)+0.092xBMI (in kg/m2)+(0.855 if woman’s mother had PE or 0 if she did not)+(–1.481 if parous without previous PE, 0.933 if parous with previous PE, or 0 if nulliparous; R2=0.153; P<0.001). For GH: Y=–5.967+0.092xBMI (in kg/m2)+(–0.822 if parous without previous PE or 0 if parous with previous PE or nulliparous; R2=0.051; P<0.001).
Patient-Specific Risk for PE and GH
The likelihood ratios for PE and GH from the log MoM MAP are shown in Table 3. For example, in an Afro-Caribbean woman in her first pregnancy, with no family history of PE, who is 28 years old, has a BMI of 20 kg/m2, does not smoke, is at 12 weeks of gestation (CRL: 65 mm), with an MAP of 85 mm Hg, the risk of developing PE is 3.9%.
For the a priori risk for PE:
- Y=–6.311+1.299 (Afro-Caribbean)+0.092x20 (BMI in kg/m2)+0 (no family history of PE)+0 (nulliparous)= –3.172
- Odds=ey=0.04191967
- A priori=odds/(1+odds)=0.04023312
For the likelihood ratio for PE:
- Measured MAP=85, log observed MAP=1.9294
- Log-expected MAP=1.8666–0.0002x65 (CRL in mm)– 0.0035 (Afro-Caribbean)+0.0005x28 (age in years)+ 0.0024x20 (BMI in kg/m2)+0 (no family history of PE)+0 (nulliparous)–0 (non smoker)=1.9121
- Log MoM MAP=1.9294–1.9121=0.0173
- Likelihood ratio for log MoM MAP of 0.0173 (see Table 3)=0.98
A posteriori risk=a priori riskxlikelihood ratio:
- risk for PE=0.04023312x0.98=0.039 or 3.9%
If the same woman had had a previous pregnancy with PE and her BMI was 35 kg/m2, her risk for PE would have been 29.2%.
Performance of Screening
The DR of PE and GH for different FPRs in screening by maternal factors only, MAP only, and by the combination of the 2 are given in Figures 2 and 3
. The areas under the receiver operating characteristic curves (AROCs) for the detection of PE were significantly higher with the combined model (AROC: 0.852) than with either history alone (AROC: 0.801; P=0.017) or MAP alone (AROC: 0.734; P<0.001). Similarly, for the detection of GH, the AROC for the combined model was significantly higher (AROC: 0.743) than with either history alone (AROC: 0.682; P=0.030) or MAP alone (AROC: 0.680; P=0.006). At a 10% FPR, the DR of PE was 43.3% for history alone, 37.5% for MAP alone, and 62.5% for combined testing, and the respective values for GH were 27.8%, 32.0%, and 41.2%.
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Discussion |
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In this screening study for hypertensive disorders of pregnancy we did the following: (1) prospectively examined a large population of pregnant women attending for routine care in a well-defined gestational age, which is now widely used for screening for chromosomal defects24,30; (2) we used a validated automated device and appropriately trained doctors to measure BP23; (3) we used strict criteria to define MAP, PE, and GH27,28; and (4) we applied a statistical approach that is widely accepted in screening for trisomy 21 to examine the performance of screening and calculate patient-specific risks.31
We found that combined first-trimester testing, for a 10% FPR, can identify 60% of those who will develop PE several months later and 40% of those who will develop GH. Taking the maternal history and recording BP are the cheapest and most ubiquitously accessible screening tools. We chose 11+0 to 13+6 weeks as the gestation for screening, because this is emerging as the first hospital visit of pregnant women at which combined sonographic and biochemical testing for chromosomal and other major defects is carried out.24 At this visit, first, a record is made of maternal characteristics; second, an ultrasound scan is carried out to determine the number of fetuses, confirm the gestation from the fetal CRL, exclude major defects, and measure the nuchal translucency thickness and other first-trimester markers of chromosomal defects; and, third, maternal blood is taken for measurement of free β-human chorionic gonadotropin and pregnancy-associated plasma protein A. It would be easy to measure the MAP of women in this same visit and use the same methodology to calculate the patient-specific risk for both chromosomal defects and PE. Essentially, factors from the maternal characteristics and history are used to calculate the a priori risk, which is multiplied by the likelihood ratio associated with biophysical and biochemical measurements to derive patient-specific risks.
In the unaffected group, which did not develop PE or GH, MAP decreased with gestation, increased with maternal age and BMI, was lower in cigarette smokers and in all of the ethnic groups other than in whites, and was higher in those with a family or personal history of PE. The risk for developing PE increased with BMI and was higher in those of Afro-Caribbean origin than in other ethnic groups and in those with a family or personal history of PE. The finding of increased MAP with age and BMI and decreased MAP in smokers is in agreement with previous reports in nonpregnant individuals.32–34 The finding that a family and personal history of PE increases the risk of developing this disorder is in agreement with previous studies reporting a 7-fold and 3-fold increase in risk for PE in women with a respective personal and family history of the disease.35 The additional finding that women with such history have a higher MAP even if they do not develop PE is compatible with the emerging evidence that a history of PE predisposes to the development of chronic hypertension.36,37 The association between black race and increased risk of PE is well documented.38 The surprising finding in our study was that, in women not developing PE or GH, the MAP was lower in women of Afro-Caribbean origin than in whites. These racial differences are the subject of further investigation.
The underlying mechanism for PE is thought to be impaired trophoblastic invasion of the maternal spiral arteries and their conversion from narrow muscular vessels to wide nonmuscular channels. There is a wide spectrum in such impaired placentation and consequent clinical presentation of the disease. Pathological studies reported that the prevalence of placental lesions in women with PE is inversely related to the gestational age at delivery.39,40 Similarly, Doppler ultrasound studies of the uterine arteries have demonstrated that the prevalence of increased impedance to flow in women developing PE is inversely related to gestation at delivery.9,41 In contrast to Doppler, we found that the mean MoM MAP at 11+0 to 13+6 weeks in those developing PE did not change significantly with gestation at delivery, and, therefore, measurement of MAP is equally effective in screening for early and late disease. Such a finding provides some support for the emerging evidence that there may be different etiologies for early and late-onset PE, with the first being primarily because of impaired placentation and the second because of maternal hemodynamic maladaptation and/or impaired glucose metabolism.42,43 The extent to which measurement of BP could be combined with other sonographic and biochemical markers for more effective screening of both early and late PE remains to be determined.
Perspectives
This study has established a methodology for the development of a screening model in the detection of PE. Maternal history and BP constitute the cornerstones of prenatal care and the foundation of any future methods for the estimation of patient-specific risk for the development of PE.
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Acknowledgments |
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Source of Funding
This study was supported by a grant from the Fetal Medicine Foundation (United Kingdom charity No. 1037116).
Disclosures
None.
Received November 7, 2007; first decision November 12, 2007; accepted November 19, 2007.
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 L. C.Y. Poon, N. A. Kametas, N. Maiz, R. Akolekar, and K. H. Nicolaides First-Trimester Prediction of Hypertensive Disorders in Pregnancy Hypertension, May 1, 2009; 53(5): 812 - 818. [Abstract] [Full Text] [PDF]
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