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Maternal plasma volume expansion and hormonal changes in women with idiopathic fetal growth retardation
Abstract
To explore the mechanisms underlying the reduced maternal plasma volume associated with idiopathic fetal growth retardation (FGR).
In 30 normotensive women with growth-retarded fetuses and 26 with normal-size fetuses, plasma volume was measured with a modified Evan's blue method. Plasma levels of atrial natriuretic peptide, plasma renin activity, aldosterone, estradiol, and progesterone, and urinary excretion of kallikrein, prostacyclin, and thromboxane A2 were measured at 34-40 weeks' gestation.
Compared with controls, gravidas with growth-retarded fetuses had a reduced plasma volume expansion (P < .01), similar atrial natriuretic peptide and plasma renin activity levels, and lower serum aldosterone (P < .001) and placental steroids (P < .03). These women also had decreased urinary kallikrein activity and prostaglandin excretion (P < .05). When both groups were combined, maternal plasma volume correlated significantly with birth weight (r = 0.53) and placental weight (r = 0.66).
Normotensive women with idiopathic FGR have reduced plasma volume expansion. Although the exact mechanisms of this change are unknown, we postulate that the lower maternal aldosterone levels and reduced levels of vasodilator substances, such as prostacyclin and kallikrein, may have a causal role.
... After ovulation, the systematic hemodynamic adaptations that occur are less but comparable to the pregnancy situation. At 6 weeks after conception, a significant PVE occurs and evidence demonstrates that (3) inadequate systematic hemodynamic adaptations are associated with adverse pregnancy outcomes, such as pre-eclampsia (PE) and fetal growth restriction (FGR) (4)(5)(6)(7)(8). ...
Objective
To study associations between the first-trimester maternal determinants of renin-angiotensin-aldosterone system (RAAS) activation and telomere length (TL) in pregnancies conceived natural and after IVF/ICSI.
Methods
In 145 pregnancies of the Rotterdam Periconception cohort renin, prorenin and aldosterone concentrations were measured in maternal blood at 9 weeks gestational age (GA). TL was measured by qPCR at 20 weeks GA.
Results
A significantly negative correlation was found between renin and TL, which was attenuated for prorenin but not observed for aldosterone. Maternal TL was significantly shorter in pregnancies conceived after in-vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) compared to natural pregnancies.
Conclusion
The negative association between first-trimester maternal renin and maternal TL, and the shorter maternal TL in women after IVF/ICSI treatment compared to natural pregnancies, substantiates the role of excessive RAAS activation.
... The fact that a hypovolemic state, which is frequently observed in FGR pregnancies, also exists prior to the onset of the disease in early pregnancy [43][44][45] and the preconception period lends credence to this hypothesis. Foo et al., most recent study starting from the time of conception, longitudinally assessed cardiovascular function in 356 spontaneously conceived pregnancies in women who appeared to be in good health [46]. ...
In recent years, there has been a growing amount of interest in the possibility that inadequate maternal hemodynamic adaptations to the pregnancy and adverse pregnancy outcomes (APOs) are connected. It has been suggested that "placental syndromes," such as preeclampsia (PE) and fetal growth restriction (FGR), may be linked to later maternal cardiovascular diseases (CVD). The two subtypes of FGR have distinct clinical and pathogenetic characteristics. It is thought that poor trophoblastic invasion of the maternal spiral arteries during placentation is a major factor in the development of early-onset PE and FGR. A pre-existing or subsequent cardiovascular impairment may play a significant role in the pathogenesis of early-onset FGR because placental functioning is dependent on the cardiovascular system of the mother. A primary abnormal placentation in the first trimester does not appear to be the factor that determines late FGR. A primary cardiovascular maladaptation in the mother may be the cause of the pathological pathway of late-onset FGR: The CV system displays a profile that is flat and remains comparable to that of non-pregnant women. A hypovolemic state could result in placental hypoperfusion, altered villous tree maturation, and altered fetal growth during the second trimester, when the placenta is already developed and has a higher functional demand. As a result, the focus of this review is on the possible connection between placentation and maternal cardiac function during pregnancy and the onset and progression of FGR. A superior comprehension of maternal hemodynamics in pregnancies confounded by FGR could get different advantages in clinical work, further developing screening and therapeutic tools.
... The fact that a hypovolemic state, which is frequently observed in FGR pregnancies, also exists prior to the onset of the disease in early pregnancy [43][44][45] and the preconception period lends credence to this hypothesis. Foo et al., most recent study starting from the time of conception, longitudinally assessed cardiovascular function in 356 spontaneously conceived pregnancies in women who appeared to be in good health [46]. ...
In recent years, there has been a growing amount of interest in the possibility that inadequate maternal hemodynamic adaptations to the pregnancy and adverse pregnancy outcomes (APOs) are connected. It has been suggested that "placental syndromes," such as preeclampsia (PE) and fetal growth restriction (FGR), may be linked to later maternal cardiovascular diseases (CVD). The two subtypes of FGR have distinct clinical and pathogenetic characteristics. It is thought that poor trophoblastic invasion of the maternal spiral arteries during placentation is a major factor in the development of early-onset PE and FGR. A pre-existing or subsequent cardiovascular impairment may play a significant role in the pathogenesis of early-onset FGR because placental functioning is dependent on the cardiovascular system of the mother. A primary abnormal placentation in the first trimester does not appear to be the factor that determines late FGR. A primary cardiovascular maladaptation in the mother may be the cause of the pathological pathway of late-onset FGR: The CV system displays a profile that is flat and remains comparable to that of non-pregnant women. A hypovolemic state could result in placental hypoperfusion, altered villous tree maturation, and altered fetal growth during the second trimester, when the placenta is already developed and has a higher functional demand. As a result, the focus of this review is on the possible connection between placentation and maternal cardiac function during pregnancy and the onset and progression of FGR. A superior comprehension of maternal hemodynamics in pregnancies confounded by FGR could get different advantages in clinical work, further developing screening and therapeutic tools.
... Jwa et al. hypothesised that a reduction in maternal hemoglobin levels from early pregnancy to mid-or late pregnancy is a proxy for plasma volume increase during pregnancy that may be protective against adverse birth outcomes including delivery of a low birthweight or small for gestational age infant [31]. Previous studies have shown that the absence of an adequate increase in plasma volume in pregnancy is associated with lower birthweight and placental weights [32][33][34]. Jwa et al. showed that women with the least reduction in hemoglobin from early to late pregnancy had a significantly increased risk of delivering a low birthweight or small for gestational age infant compared to women with the intermediate or greatest reduction [31]. This may explain the negative association between late maternal hemoglobin and birthweight from our study-there was an approximate 1 g/dL mean drop in maternal hemoglobin from 13 to 28 weeks' gestation (Table 2) which may have resulted in a suboptimal plasma volume expansion in our women throughout their pregnancies. ...
Purpose
Dietary micronutrient intakes of iron, folate and vitamin B12 are known to influence hemoglobin. Low maternal hemoglobin (maternal anemia) has been linked to low birthweight and other adverse health outcomes in the fetus and infant. Our primary aim was to explore relationships between maternal dietary micronutrient intakes, maternal full blood count (FBC) parameters and fetal abdominal circumference (AC) and estimated fetal weight (EFW) growth trajectories. Secondarily, we aimed to assess relationships between maternal dietary micronutrient intakes, maternal hemoglobin values and placental weight and birthweight.
Methods
Mother–child pairs ( n = 759) recruited for the ROLO study were included in this analysis. Maternal dietary micronutrient intakes were calculated from food diaries completed during each trimester of pregnancy. FBC samples were collected at 13- and 28-weeks’ gestation. Fetal ultrasound measurements were recorded at 20- and 34-weeks’ gestation. Growth trajectories for AC and EFW were estimated using latent class trajectory mixture models.
Results
Dietary intakes of iron and folate were deficient for all trimesters. Mean maternal hemoglobin levels were replete at 13- and 28-weeks’ gestation. Dietary iron, folate and vitamin B12 intakes showed no associations with fetal growth trajectories, placental weight or birthweight. Lower maternal hemoglobin concentrations at 28 weeks’ gestation were associated with faster rates of fetal growth and larger placental weights and birthweights.
Conclusion
The negative association between maternal hemoglobin at 28 weeks’ gestation and accelerated fetal and placental growth may be due to greater consumption of maternal iron and hemoglobin by fetuses’ on faster growth trajectories in addition to placental biochemical responses to lower oxygen states.
... Pregnant women with the lowest Hb reduction from early to late pregnancy had an increased risk of LBW and SGA compared with women with an intermediate Hb reduction [15,24]. Changes in Hb during pregnancy were significantly correlated with changes in plasma volume [43,49]. A smaller decrease in maternal Hb from the first trimester may indicate a reduction in plasma volume expansion, which may impair fetoplacental circulation and increase the risk of LBW and SGA [41]. ...
Maternal hemoglobin (Hb) is related to nutritional status, which affects neonatal birth weight. However, it is very common for maternal Hb to fluctuate during pregnancy. To evaluate the associations of maternal Hb in different time points and its changes during pregnancy with neonatal birth weight, small for gestational age (SGA)/low birth weight (LBW) and large for gestational age (LGA)/macrosomia, we conducted this study by using data from the Electronic Medical Record System (EMRS) database of Zhoushan Maternal and Child Care Hospital in Zhejiang province, China. The pregnancy was divided into five periods: first, early-second, mediate-second, late-second, early-third and late-third trimesters; we further calculated the maternal Hb changes during pregnancy. Overall, the socio-demographic characteristics, health-related information and childbirth-related information of 24,183 mother–infant pairs were obtained. The average Hb concentration during the different periods were 123.95 ± 10.14, 117.95 ± 9.84, 114.31 ± 9.03, 113.26 ± 8.82, 113.29 ± 8.68 and 115.01 ± 8.85 g/L, respectively. Significant dose–response relationships between maternal Hb and birth weight were observed in the first, late-second and later trimesters (p non-linear < 0.05). Maternal Hb < 100 g/L was related to a high risk of LGA/macrosomia in the late-second (OR: 1.47, 95% CI: 1.18, 1.83) and later trimesters; additionally, high maternal Hb (>140 g/L) increased the risk of SGA/LBW in the first (OR: 1.26, 95% CI: 1.01, 1.57) and late-third trimesters (OR: 1.96, 95% CI: 1.20, 3.18). In addition, the increase in maternal Hb from the late-second to late-third trimesters had a positive correlation with SGA/LBW. In conclusion, maternal Hb markedly fluctuated during pregnancy; the negative dose–response association of maternal Hb in the late-second and third trimesters, and Hb change during pregnancy with neonatal birth weight outcomes were observed, respectively. Furthermore, the phenomenon of high Hb in the first trimester and after the late-second trimester and the increase of maternal Hb from the late-second to late-third trimesters more significantly increasing the risk of SGA/LBW should especially be given more attention. Its biological mechanism needs to be further explored.
Hypertensive disorders of pregnancy continue to be significant contributors to adverse perinatal outcome and maternal mortality, as well as inducing life-long cardiovascular health impacts that are proportional to the severity and frequency of pregnancy complications. The placenta is the interface between the mother and fetus and its failure to undergo vascular maturation in tandem with maternal cardiovascular adaptation by the end of the first trimester predisposes to hypertensive disorders and fetal growth restriction. While primary failure of trophoblastic invasion with incomplete maternal spiral artery remodeling has been considered central to the pathogenesis of preeclampsia, cardiovascular risk factors associated with abnormal first trimester maternal blood pressure and cardiovascular adaptation produce identical placental pathology leading to hypertensive pregnancy disorders. Outside pregnancy blood pressure treatment thresholds are identified with the goal to prevent immediate risks from severe hypertension >160/100 mm Hg and long-term health impacts that arise from elevated blood pressures as low as 120/80 mm Hg. Until recently, the trend for less aggressive blood pressure management during pregnancy was driven by fear of inducing placental malperfusion without a clear clinical benefit. However, placental perfusion is not dependent on maternal perfusion pressure during the first trimester and risk-appropriate blood pressure normalization may provide the opportunity to protect from the placental maldevelopment that predisposes to hypertensive disorders of pregnancy. Recent randomized trials set the stage for more aggressive risk-appropriate blood pressure management that may offer a greater potential for prevention for hypertensive disorders of pregnancy.
Key Points
Fetal macrosomia is associated with a number of health complications for both mother and infant in the immediate, short, and long-term. Maternal obesity and excessive gestational weight gain (GWG) have long been associated with fetal macrosomia, however the impact of maternal lifestyle factors such as dietary intake and energy balance, in combination with the timing and composition of weight gain, have been less studied. It is also clear that although maternal obesity and excessive GWG increase the risk of fetal macrosomia independently, the risk is magnified with the presence of both risk factors, suggesting that interventions to control GWG may be particularly important for obese women. Association studies examining the relationship between fetal nutrient availability, epigenetic modifications, and infant anthropometrics are also required. This review provides an overview of the current evidence examining the role of maternal lifestyle factors on the prevalence of fetal macrosomia and identifies areas where further research is required in order to inform the design of appropriate intervention strategies.
Measurements of blood volume were carried out between 24 and 40 weeks of gestation in 20 multiparous patients with chronic hypertension and pregnancy. Hypertensive patients had both reduced blood volume and infants of smaller weight (p less than 0.01) than nonhypertensive control subjects. There was a significant difference (p less than 0.01) in the degree of blood volume expansion in hypertensive mothers who were delivered of infants who were adequate for gestational age (AGA), term, or premature, compared to those who were delivered of infants who were small for gestational age (SGA) or stillborn. Classification of chronic hypertension during pregnancy according to the American Committee on Maternal Welfare classification or according to severity of the hypertension was of no value in identifying the mothers at risk of delivering intrauterine growth-retarded infants. However, failure in achieving a blood volume expansion of at least 60 c.c. per kilogram clearly identified those pregnancies leading to growth retardation and fetal death. The decrease or lack of intravascular volume expansion was reflected in the presence of creatinine clearance values at nonpregnant levels in the mothers who were delivered of SGA infants and in a significant reduction below the nonpregnant levels in those who were delivered of stillborn infants. These data suggest that measurement of blood volume and endogenous creatinine clearance in patients with chronic hypertension and pregnancy is a useful parameter in the identification of those patients who will have a poor fetal outcome.