Maternal Blood Pressure In Pregnancy Research Articles

Calcium supplementation on lowering blood pressure in pregnant women with hypertension: A meta-analysis

<p><strong><em>Background:</em></strong><em> Hypertension in pregnancy causes 10% of pregnancy disorders worldwide which results in maternal morbidity and mortality of 9-26% and the incidence of premature births as much as 15% worldwide. From the results of previous meta-analysis, there is a relationship between calcium intake and the incidence of preeclampsia by consuming 1500-2000mg calcium during pregnancy, it is necessary to add calcium supplements to pregnant women because not all calcium intake in pregnant women from food is sufficient to meet calcium needs. </em></p><p><strong><em>Objectives:</em></strong><em> Analyzing research studies on the effect of calcium on systolic blood pressure in pregnant women with hypertension in pregnancy, Analyzing research studies on the effect of calcium on diastolic blood pressure in pregnant women with hypertension in pregnancy.</em></p><p><strong><em>Methods:</em></strong><em> Meta analysis by searching 24 research studies from 5 databases (Pubmed, Science Direct, Google Schoolar, Elsevier, and Proquest) using Randomized Control Trial (RCT), Experimental, and Cohort, published in 2013-2020.</em></p><p><strong><em>Results:</em></strong><em> the results of the analysis of 5 studies involving 945 selected pregnant women with an average use of moderate doses (500 mg / day during the study) were divided into 2 groups. Providing calcium intervention since 20 weeks of gestation showed that calcium supplementation had a decreasing impact on maternal blood pressure in pregnancy. Analysis showed a difference in blood pressure in mothers with hypertension in pregnancy compared to mothers who did not consume calcium.</em></p><p><strong><em>Conclusions:</em></strong><em> The use of calcium supplements during pregnancy can reduce blood pressure and prevent preeclampsia. The recommended dose is 500 mg/day from 20 weeks of gestation with mothers at risk of preeclampsia. Health workers need to ensure that pregnant women comply with the calcium consumption rules given so that the management recommendations can be carried out properly</em></p>

Blood Pressure and Angiogenic Markers in Pregnancy: Contributors to Pregnancy-Induced Hypertension and Offspring Cardiovascular Risk.

Pregnancy-induced hypertension is a severe pregnancy complication, increasing risk of long-term cardiovascular disease in mothers and offspring. We hypothesized that maternal blood pressure in pregnancy associated with offspring blood pressure; that the associations were sex-specific; and that maternal circulating placental angiogenic markers (PlGF [placental growth factor] and sFlt-1 [soluble fms-like tyrosine kinase-1]) mediated this relationship. We analyzed data from 2434 women and 2217 children from the Odense Child Cohort, a prospective Danish cohort study. Offspring blood pressure trajectory from 4 months to 5 years was highly associated to maternal first, second, and third trimester blood pressure, and mean blood pressure in pregnancy, independent of maternal and offspring covariates. There were offspring sex-specific associations: Girls from mothers in the highest quartile of first and third trimester blood pressure had significantly higher systolic blood pressure at 5 years than the rest of the cohort (mean difference±SEM: 1.81±0.59 and 2.11±0.59 mm Hg, respectively, all P<0.01); whereas boys had significantly higher diastolic blood pressure at 5 years (mean difference±SEM: 1.11±0.45 and 1.03±0.45, respectively, all P<0.05). Concentrations of PlGF at gestational week 28 correlated inversely to maternal gestational blood pressure trajectory, independent of the diagnosis of pregnancy-induced hypertension, adjusted β coefficients (95% CI) for predicting systolic blood pressure (SBP): -3.18 (-4.66 to -1.70) mm Hg, for predicting diastolic blood pressure (DBP): -2.48 (-3.57 to -1.40) mm Hg. In conclusion, maternal gestational blood pressure predicted offspring blood pressure trajectory until 5 years in a sex-differential manner. Furthermore, subtle alterations in blood pressure in early pregnancy preceded hypertension or preeclampsia, and PlGF was a mediator of cardiovascular health in pregnancy.

DASH (Dietary Approaches to Stop Hypertension) dietary pattern and maternal blood pressure in pregnancy.

High blood pressure (BP) in pregnancy is associated with significant adverse outcomes. In nonpregnant populations, the DASH (Dietary Approaches to Stop Hypertension) diet is associated with reductions in blood pressure. The present study investigated the relationship between the DASH dietary pattern and maternal BP in pregnancy. This is an observational study of 511 women who participated in the ROLO study (Randomized cOntrol trial of LOw glycaemic index diet for the prevention of recurrence of macrosomia), 2007-2011, Dublin, Ireland. Auscultatory blood pressure, systolic blood pressure (SBP) and diastolic blood pressure (DBP) measurements were taken. Mean arterial pressure (MAP) was calculated. Dietary intakes were recorded using 3-day food diaries in each trimester. DASH scoring criteria were used to score and rank participants from low to high intakes of foods recommended in the DASH diet. Statistical analysis using analysis of variance and multiple linear regression were used to determine the relationship between maternal BP and DASH scores. Dietary intake more closely resembling the DASH dietary recommendations throughout pregnancy was associated with a lower DBP (mmHg) in trimesters 1 [B: -0.70; 95% confidence interval (CI)=-1.21 to -0.18] and 3 (B: -0.68; 95% CI=-1.19 to -0.17), as well as lower MAP (mmHg) in trimesters 1 (B: -0.78; 95% CI=-1.33 to -0.25) and 3 (B: -0.54; 95% CI=-1.04 to -0.04), controlling for body mass index, age, education, energy intake and intervention grouping. The DASH dietary pattern was associated with lower maternal BP in pregnancy among healthy women without hypertensive disorders of pregnancy. Despite the observational nature of these findings, the results demonstrate the potential for healthcare professionals to intervene to promote cardiovascular health in pregnancy.

Age at menarche and blood pressure in pregnancy

Abstract Objectives To investigate whether age at menarche is related to maternal blood pressure in pregnancy and, if so, whether obesity and insulin resistance can modify the associations. Study design Analysis of data collected from 438 pregnant women from the longitudinal and prospective Cambridge Baby Growth Study. Main outcome Testing associations between questionnaire-derived age at menarche and blood pressure measurements in pregnancy collected from hospital notes, and investigating whether any associations were altered by maternal pre-pregnancy body mass index (BMI) and insulin resistance. Measures Mean arterial blood pressure at four time points across pregnancy, age at menarche, (Homeostasis Model Assessment) insulin resistance around week 28 of pregnancy. Results For each increased year in age at menarche there was a drop in mean arterial blood pressure (mmHg) of 0.6 at 11.9 weeks, 0.9 at 31.4 and 37.0 weeks, and 0.4 at 38.8 weeks (a maximal difference of over 7 mmHg across extremes of AAM). Each association was attenuated by both maternal pre-pregnancy BMI and insulin resistance. Conclusions Age at menarche is negatively associated with future blood pressure in pregnancy, so those with the earliest age at menarche have the highest blood pressures. Either these associations may be mediated by links between age at menarche and obesity/insulin resistance, or there may be a confounder (e.g. systemic inflammation) that links age at menarche to each of them.

Dose-response relationship between maternal blood pressure in pregnancy and risk of adverse birth outcomes: Ma'anshan birth cohort study.

This study depicts the dose-response relationship between blood pressure (BP) during pregnancy and adverse birth outcomes in different trimesters. We used restricted cubic spline to quantify the dose-response relationship between maternal BP in different trimesters and risk of adverse birth outcomes (small for gestational age, SGA; and pre-term birth, PTB). The data were from the Ma'anshan birth cohort study in China (N = 3273). Risk of SGA and PTB. There were dose-response associations of both systolic blood pressure (SBP) and diastolic blood pressure (DBP) with risk of SGA in the third trimester and with PTB in both second and third trimesters. In the third trimester, compared with SBP of 120 mmHg, the odds ratios (ORs) and 95% confidence intervals (CI) of SGA were 1.12 (1.01-1.19), 1.32 (1.10-1.60), 1.65 (1.20-2.27) and 2.05 (1.30-3.24) for SBP of 125, 130, 135 and 140 mmHg, respectively. The corresponding ORs and 95% CIs of PTB were 1.15 (1.00-1.32), 1.59 (1.28-1.98), 2.35 (1.66-3.33) and 3.47 (2.10-5.73), respectively. Compared with DBP of 70 mmHg, the ORs and 95% CIs of SGA were 1.44 (1.16-1.78) and 3.04 (2.06-4.50) for DBP of 80 and 90 mmHg, respectively. The corresponding ORs and 95% CIs of PTB were 1.32 (0.93-1.90) and 3.58 (2.21-5.78), respectively. A consistent set of dose-response relationships between maternal BP and adverse birth outcomes were observed. Most importantly, we found that moderately elevated maternal BP, even within a normal range, increased the risk of adverse birth outcomes.

Is infant arterial stiffness associated with maternal blood pressure in pregnancy? Findings from a UK birth cohort (Baby VIP study).

BackgroundIn adults, arterial stiffness measured by pulse wave velocity (PWV) is regarded as a predictor of cardiovascular disease. Infant vascular development depends on factors related to pregnancy, including maternal blood pressure (BP). This study assessed the association between maternal BP in pregnancy and infant brachio-femoral PWV at age 2–6 weeks.MethodsThe Baby Vascular health and Iron in Pregnancy (Baby VIP) study is a birth cohort which measured PWV and heart rate (HR) in 284 babies in Leeds, UK, at 2–6 weeks after birth. Maternal BP measurements at 12 and 36 weeks gestation was collected from antenatal clinical records. Multivariable linear regression models assessed associations between maternal systolic and diastolic BPs, and BP change from booking to 36 weeks, with infant PWV adjusting for covariables at both mother and baby level.ResultsThere was no evidence of an association between infant PWV and maternal systolic BP at booking (adjusted regression coefficient -0.01 m/s per 10mmHg, 95% CI -0.11, 0.14, p = 0.84) or at 36 weeks (adjusted regression coefficient 0.00 m/s per 10mmHg, 95% CI -0.12, 0.11, p = 0.95). Change between 12 and 36 weeks gestation of more than 30 mmHg in systolic BP or 15 mmHg in diastolic BP was also not associated with infant PWV. There was an inverse relationship between infant HR and infant PWV (regression coefficient -0.14 m/s per 10 bpm, 95% CI -0.22, -0.05, p<0.01).ConclusionsThis study has shown no evidence of association between infant PWV at 2–6 weeks of age and maternal BP in early or late pregnancy. Infant HR was inversely associated with infant PWV. Further studies are required to determine the predictors of infant PWV as well as the importance and long term implications of PWV measurements in infants.

CHIPS-Child: Testing the developmental programming hypothesis in the offspring of the CHIPS trial.

As a follow-up to the CHIPS trial (Control of Hypertension In Pregnancy Study) of 'less tight' (versus 'tight') control of maternal blood pressure in pregnancy, CHIPS-Child investigated potential developmental programming of maternal blood pressure control in pregnancy, by examining measures of postnatal growth rate and hypothalamic-pituitary adrenal (HPA) axis activation. CHIPS follow-up was extended to 12 ± 2 months corrected post-gestational age for anthropometry (weight, length, head/waist circumference). For eligible children with consent for a study visit, we collected biological samples (hair/buccal samples) to evaluate HPA axis function (hair cortisol levels) and epigenetic change (DNA methylation analysis of buccal cells). The primary outcome was 'change in z-score for weight' between birth and 12 ± 2 mos. Secondary outcomes were hair cortisol and genome-wide DNA methylation status. Of 683 eligible babies, 183 (26.8%) were lost to follow-up, 83 (12.2%) declined, 3 (0.4%) agreed only to ongoing contact, and 414 (60.6%) consented. 372/414 (89.9%) had weight measured at 12mos. In 'less tight' (vs. 'tight') control, the primary outcome was similar [-0.26 (-0.53, +0.01); p = 0.14, padjusted = 0.06]; median (95% confidence interval) hair cortisol (N = 35 samples) was lower [-496 (-892, -100) ng/g; p = 0.02], and buccal swab DNA methylation (N = 16 samples) was similar. No differences in growth rate could be demonstrated up to 5 years. Results demonstrate no compelling evidence for developmental programming of growth or the HPA axis. Clinicians should look to the clinical findings of CHIPS to guide practice. Researchers should seek to replicate these findings and extend outcomes to paediatric blood pressure and neurodevelopment.

Clinical Implications

HomeHypertensionVol. 68, No. 6Clinical Implications Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBClinical Implications Originally published1 Dec 2016https://doi.org/10.1161/HYPERTENSIONAHA.116.08492Hypertension. 2016;68:1321Cardiovascular Health and Masked Hypertension (p 1475)Download figureDownload PowerPointPrevious data from the Jackson Heart Study indicate that the prevalence of masked hypertension exceeds 50% in African Americans. Masked hypertension is associated with 2× the risk for cardiovascular disease. Data suggest that individuals with prehypertension have a high probability of having prevalent masked hypertension. Despite the importance of masked hypertension on cardiovascular outcomes, there have been few studies investigating risk factors for masked hypertension. Identifying modifiable risk factors for masked hypertension may provide an approach to prevent its development and reduce its prevalence. In the current study, Bromfield et al report that better cardiovascular health (ideal levels of body mass index, physical activity, nonsmoking, diet, clinic blood pressure, total cholesterol, and fasting glucose) was associated with a lower prevalence of masked daytime, nighttime, and 24-hour hypertension, and any masked hypertension were less prevalent among participants with. These results provide evidence that improving and maintaining cardiovascular health may lower the probability of having masked hypertension in African Americans. Although randomized clinical trials are needed to determine the efficacy of lifestyle interventions on delaying or preventing masked hypertension, clinicians should continue to encourage their patients to improve their cardiovascular risk factors through lifestyle modification, specifically by improving physical activity and diet and stopping cigarette smoking that can result in lower clinic blood pressure levels and maintain better cardiovascular health.Fetal Imprinted Genes and Maternal Blood Pressures (p 1459)Download figureDownload PowerPointEpidemiological studies suggest that gestational hypertension has both environmental and genetic pathogenic components. Defining its genetic risk factors may lead to improvements in pregnancy risk assessment and novel therapeutic targets. Known maternal genetic risk variants only account for a small fraction of the total genetic risk of gestational hypertension. The fetal genome may also contribute to that risk. Petry et al tested fetal variants in imprinted genes for associations with maternal blood pressure in pregnancy because these genes are thought to mediate the separate reproductive genetic needs of each parent. Using 2 birth cohorts from Cambridge, United Kingdom, they found 7 variants that were significantly associated with maternal blood pressure in the second half of pregnancy. In meta-analyses with additional independent data from the Hyperglycemia and Adverse Pregnancy Outcome Study, one of these variants, maternally transmitted fetal rs10139403, was associated with maternal mean arterial blood pressure at the genome-wide level—the first such finding of its kind. A composite fetal imprinted gene allele score constructed from the 7 key variants was associated with both maternal mean arterial blood pressure in the second half of pregnancy at the genome-wide level (explaining up to 8.7% of its variance) and gestational hypertension (each additional risk allele contributing an additional 50% to the risk). These data support the concept that fetal imprinted genes are related to the development of gestational hypertension.Medication Use in Resistant Hypertension, 2008 to 2014 (p 1349)Download figureDownload PowerPointCurrent recommendations for treatment-resistant hypertension (TRH) include optimizing medical therapy such as thiazide diuretics and aldosterone antagonists. But the extent to which such recommendations have been implemented is not well studied, and little is known about longitudinal trends in antihypertensive use, generally, among patients with TRH. We analyzed antihypertensive use in US adults (aged 18–65 years) with apparent TRH, defined as the concurrent use of ≥4 antihypertensive agents, from July 2008 to December 2014 using Marketscan commercial claims data. Over this time period, thiazide diuretic use was generally stable and prevalent in >80% of TRH episodes. Hydrochlorothiazide predominated among thiazides for all time periods, whereas chlorthalidone use increased modestly from 3.8% to 6.3% of all TRH episodes from 2008 to 2014. Aldosterone antagonist prevalence increased by 2.9% (7.3%–10.2%) over the same time period, driven almost exclusively by greater spironolactone use (Figure). Likewise, dihydropyridine calcium channel blocker and β-blocker use increased over the study period, whereas angiotensin-converting enzyme inhibitor use decreased. Concurrent angiotensin-converting enzyme inhibitor and angiotensin receptor blocker use declined from 17.7% (2008) to 6.3% (2014) of TRH episodes, whereas the use of preferred 3-drug regimens (diuretic, dihydropyridine calcium channel blocker, and ACE-I or angiotensin receptor blocker, but not both) increased from 50.8% to 64.6%. Our results highlight persistent, infrequent use of recommended therapies and suggest a need for increased efforts targeting evidence-based approaches. Previous Back to top Next FiguresReferencesRelatedDetails December 2016Vol 68, Issue 6 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.116.08492 Originally publishedDecember 1, 2016 PDF download Advertisement

17 Is maternal blood pressure during pregnancy associated with infant arterial stiffness?

Introduction In adults, arterial stiffness measured by pulse wave velocity (PWV) is regarded as a predictor of cardiovascular disease [1]. This association is less well established in infants, however. Infant and childhood vascular development is dependent on several factors related to the pregnancy, including maternal blood pressure (BP) with one study finding an inverse relationship between BP and neonatal aortic PWV at 1–3days [2]. Objective To assess the association between maternal BP in pregnancy and infant brachio-femoral PWV at age 2–6weeks. Methods The Baby VIP study recruited mother-baby pairs from postnatal wards at Leeds Teaching Hospitals NHS Trust. PWV was measured non-invasively in 284 babies at a home visit 2–6weeks after recruitment using the Vicorder device. Maternal BP at booking and at 36weeks gestation, along with other co-variables, were collected from delivery and antenatal notes. Multivariable linear regression models were used to link maternal systolic and diastolic BPs, and BP change from booking to 36weeks with PWV. Results At booking, the mean maternal systolic BP was 112mmHg (standard deviation (s.d) 12) and diastolic BP was 67mmHg (s.d 10). At 36weeks gestation, mean maternal systolic BP was 116.3mmHg (s.d 15) and diastolic BP was 70.8mmHg (s.d 12). Mean infant PWV was 6.7m/s (s.d 1.3). PWV was not significantly associated with hypertension in pregnancy (at booking or at 36weeks) in univariate analysis, where hypertension was defined as systolic BP⩾140mmHg or diastolic BP⩾90mmHg, or a rise in systolic BP of ⩾30mmHg or rise in diastolic BP of ⩾15mmHg from booking to 36weeks ( p >0.05). There was no association between infant PWV and maternal systolic BP at 36 weeks assessed as a continuous variable (regression co-efficient 0.003m/s, 95% confidence intervals (CI) −0.01, 0.01, p =0.6) adjusted for pregnancy factors including maternal age, ethnicity, history of gestational diabetes, pre-eclampsia, anaemia, BMI and infant factors including baby's age, position, whether sleep or awake at the time of measurement, and prematurity. There was no association between infant PWV and a ⩾30mmHg rise in systolic BP at 36 weeks from booking (adjusted regression co-efficient −0.4m/s, 95% CI −1.1, 0.41, p =0.4). Conclusions This study has shown that there is no evidence of any associations between infant PWV and hypertension or maternal BP during pregnancy. We demonstrate the feasibility and acceptability of using PWV in early infancy. However, further studies are required to determine the predictors of infant PWV, the significance and long term implications of PWV measurements in infants.

51 Differences in sodium intake determine the blood pressure phenotype in pregnant rats

Background In pregnancy, plasma volume expansion by high aldosterone levels is crucial to prevent placental ischaemia, a condition linked to maternal arterial hypertension. Objective We hypothesise that an adapted salt intake will further lead to a favourable maternal blood pressure response. Methods Sprague–Dawley rats were followed by blood pressure telemetry and metabolic measurements before mating and throughout pregnancy in four experimental groups receiving either normal (NS; 0.4%), high (HS; 8%), low (LS; 0.01%), or high (8%) for the first 14 d of pregnancy followed by a switch to low Na + diet (0.01%) until day 20 (HS/LS). On day 20 the animals were sacrificed. Food, water and Na + balance was recorded. Results In pregnancy, Na + intake ( p = 0.02) and retention ( p = 0.004) increased already in NS conditions. The ratio of Na + intake vs. excretion was high in pregnant rats on NS ( p = 0.015) and LS ( p = 0.008 vs. non-pregnant) diet and low ( p p = 0.004–0.044 vs. non-pregnant) as compared to NS diet ( p Conclusions Pregnancy determines the response to dietary changes in salt intake aiming to preserve salt thus overcoming periods of low salt availability as shown in our HS/LS model. Increased salt intake reduces maternal blood pressure in pregnancy. Though the exact dose and temporal relationship needs to be elucidated, these results highlight the important role of environmental factors, such as salt, for a successful pregnancy.

Fetal growth restriction and risk of cerebral palsy in singletons born after at least 35 weeks’ gestation

The objective of the study was to improve the understanding of etiological paths to cerebral palsy (CP) that include fetal growth restriction by examining factors associated with growth restriction that modify CP risk. In a total population of singletons born at or after 35 weeks, there were 493 children with CP and 508 matched controls for whom appropriateness of fetal growth could be estimated. Fetal growth was considered markedly restricted if birthweight was more than 2 SD below optimal for gender, gestation, maternal height, and parity. We examined maternal blood pressure in pregnancy, smoking, birth asphyxia, and major birth defects recognized by age 6 years as potential modifiers of CP risk in growth-restricted births. More than 80% of term and late preterm markedly growth-restricted singletons were born following a normotensive pregnancy and were at statistically significantly increased risk of CP (odds ratio, 4.81; 95% confidence interval, 2.7-8.5), whereas growth-restricted births following a hypertensive pregnancy were not. Neither a clinical diagnosis of birth asphyxia nor potentially asphyxiating birth events occurred more frequently among growth-restricted than among appropriately grown infants with CP. Major birth defects, particularly cerebral defects, occurred in an increasing proportion of CP with increasing growth deficit. The factor most predictive of CP in growth-restricted singletons was a major birth defect, present in 53% of markedly growth-restricted neonates with later CP. Defects observed in CP were similar whether growth restricted or not, except for an excess of isolated congenital microcephaly in those born growth restricted. The highest observed CP risk was in infants with both growth restriction and a major birth defect (8.9% of total CP in this gestational age group, 0.4% of controls: odds ratio, 30.9; 95% confidence interval, 7.0-136). The risk of CP was increased in antenatally growth-restricted singletons born at or near term to normotensive mothers. In growth-restricted singletons, a major birth defect was the dominant predictor, associated with a 30-fold increase in odds of CP. Identification of birth defects in the growth-restricted fetus or neonate may provide significant prognostic information.

Association of maternal blood pressure in pregnancy with blood pressure of their offspring through adolescence.

This article looks at the association of maternal blood pressure with the blood pressure of the offspring from birth to childhood. The Barker hypothesis states that maternal and "in utero" attributes during pregnancy affect a child's cardiovascular health throughout life. We present an analysis of a unique dataset that consists of three distinct developmental processes: maternal cardiovascular health during pregnancy; fetal development; and child's cardiovascular health from birth to 14 years. This study explored whether a mother's blood pressure reading in pregnancy predicts fetal development and determines if this in turn is related to the future cardiovascular health of the child. This article uses data that have been collected prospectively from a Jamaican cohort which involves the following three developmental processes: (1) maternal cardiovascular health during pregnancy which is the blood pressure and anthropometric measurements at seven time-points on the mother during pregnancy; (2) fetal development which consists of ultrasound measurements of the fetus taken at six time-points during pregnancy; and (3) child's cardiovascular health which consists of the child's blood pressure measurements at 24 time-points from birth to 14 years. The inter-relationship of these three processes was examined using linear mixed effects models. Our analyses indicated that attributes later in childhood development, such as child's weight, child's baseline systolic blood pressure (SBP), age and sex, predict the future cardiovascular health of children. The results also indicated that maternal attributes in pregnancy, such as mother's baseline SBP and SBP change, predicted significantly child's SBP over time.

The potential impact of the fetal genotype on maternal blood pressure during pregnancy.

The heritability of pregnancy-induced hypertension (encompassing both gestational hypertension and preeclampsia) is around 0.47, suggesting that there is a genetic component to its development. However, the maternal genetic risk variants discovered so far only account for a small proportion of the heritability. Other genetic variants that may affect maternal blood pressure in pregnancy arise from the fetal genome, for example wild-type pregnant mice carrying offspring with Cdkn1c or Stox1 disrupted develop hypertension and proteinuria. In humans, there is a higher risk for preeclampsia in women carrying fetuses with Beckwith-Wiedemann syndrome (including those fetuses with CDKN1C mutations) and a lower risk for women carrying babies with trisomy 21. Other risk may be associated with imprinted fetal growth genes and genes that are highly expressed in the placenta such as GCM1. This article reviews the current state of knowledge linking the fetal genotype with maternal blood pressure in pregnancy.

Maternal Blood Pressure in Pregnancy and Stillbirth: A Case-Control Study of Third-Trimester Stillbirth

An immense body of literature on the effects of hypertension on perinatal morbidity and mortality exists, but only a handful of studies have reported adverse outcomes associated with low maternal blood pressure during pregnancy. This study aimed to investigate if there is an increased risk of fetal loss associated with hypotension during pregnancy. A matched case-control study of stillbirth and maternal blood pressure was conducted in which maternal blood pressures for a total of 124 pregnancies culminating in stillbirth were compared with maternal blood pressures in 243 (matched) pregnancies resulting in a liveborn infant. Women whose diastolic blood pressures fell in a borderline range (60 to 70 mm Hg) were consistently at greater risk of stillbirth relative to normotensive pregnancies. Women who had three or more mean arterial pressure values < or = 83 mm Hg during the course of their pregnancy were at nearly twice the risk of stillbirth (odds ratio 1.78; 95% confidence interval [CI] 1.06 to 2.99; P = 0.03). Systolic hypotension was not significantly associated with stillbirth, but proportionately more control women were noted to have systolic hypertension (SBP > or = 130 mmHg) than cases, and the adjusted odds of stillbirth in women who were hypertensive at either their first or last antenatal visit or whose antenatal average SBP was > or = 130 mm Hg were all very close to 0.4 (95% CI 0.37 to 0.43; P = 0.02 to 0.03) relative to normotensives. We concluded that maternal hypotension, particularly borderline hypotension, may be a contributory risk factor for stillbirth. Women with hypertension in pregnancy may now be at a decreased risk of stillbirth as a result of the close care and treatment they receive.

Maternal blood pressure in pregnancy, birth weight, and perinatal mortality in first births: prospective study

Objective To investigate the relation of diastolic blood pressure in pregnancy with birth weight and perinatal mortality.Design Prospective study.Setting 15 maternity units in one London health region, 1988-2000.Participants 210 814...

24‐hour blood pressure monitoring to evaluate the effects of nifedipine in pre‐eclampsia and in chronic hypertension in pregnancy

To investigate the effect of 7 to 14 days of therapy with nifedipine (sustained-release preparation) on the 24-hour blood pressure patterns of pregnant women with pre-eclampsia or chronic hypertension, and to test the utility of blood pressure monitoring in modulating the timing and dosage of the drug. 24-hour automatic blood pressure monitoring of pregnant women with pre-eclampsia or chronic hypertension before and after nifedipine treatment. Centre for Prevention, Diagnosis and Treatment of Hypertension in Pregnancy, University of Turin, Italy. Sixteen pregnant women with pre-eclampsia and 17 with chronic hypertension. 24-hour blood pressure monitoring was performed before the beginning of the therapy and after 7 to 14 days of treatment with sustained-release nifedipine. Chronobiological analysis of systolic and diastolic blood pressure values was performed; MESOR, amplitude, acrophase, hyperbaric index, percent time elevation and significance of rhythm were calculated before and after treatment. 6336 blood pressure measurements were analysed. Systolic and diastolic MESOR values were significantly decreased after nifedipine treatment both in pre-eclampsia and in chronic hypertension. However, the antihypertensive effect of nifedipine in pre-eclampsia was especially pronounced during evening and night, while in chronic hypertension it was more constant during the 24-hour period. 24-hour blood pressure monitoring allowed adjustment, when necessary, to the timing and dosage of nifedipine in accordance with the blood pressure patterns of each patient, using the hyperbaric index and percent time elevation as objective parameters for the evaluation of treatment efficacy. 24-hour blood pressure monitoring is a good method to optimise treatment, and confirms that nifedipine is useful for the control of maternal blood pressure in pregnancy.

Nifedipine does not adversely affect uteroplacental blood flow in the hypertensive term-pregnant rat

The short-term effect of the calcium channel blocker, nifedipine, on maternal hemodynamics and organ perfusion was investigated in 12 hypertensive term-pregnant, spontaneously hypertensive rats by means of the radioactive-labeled microsphere technique. The normal fall in blood pressure during pregnancy was prevented by reducing litter size to two conceptuses on day 7 of gestation. Nifedipine (200 μg/kg) effectively lowered mean arterial pressure 25% by decreasing total peripheral resistance 38%. Cardiac output was increased 15%. Blood flows to the splanchnic region and the reproductive organs were increased after nifedipine administration. The increase in blood flow to the reproductive organs was the result of increased ovarian and uterine wall perfusion caused by large reductions in vascular resistances. Placental blood flow was not significantly altered, but resistance was decreased. Thus, the use of nifedipine to lower maternal blood pressure in pregnancy complicated by extreme hypertension does not necessarily decrease uteroplacental perfusion.

Maternal blood pressure in pregnancy and newborn irritability

The neonatal period is being recognized as an important period for the development of patterns of interaction between mother and infant, and infant state has been shown to have a significant impact on mother--infant interactions. A major dimension of infant state, with implications for this interaction and for the development of later behaviour disorders, is the infant's irritability. Research with Navajo, Malay, Chinese and Tamil mothers and infants showed that normal variation in maternal blood pressure during pregnancy was related to newborn irritability as assessed with the Brazelton Scale. This relationship is discussed in terms of possible underlying mechanisms.