Lower Maternal Blood Pressure Research Articles

Influence of Light Intensity exercise During Pregnancy on Fetal Echocardiographic and Maternal Cardiovascular Measures

Background: Although moderate intensity maternal exercise is recommended during pregnancy, most women do not achieve this level. Objective: This study aimed to determine the effects of supervised maternal light-intensity exercise on fetal cardiovascular measures in the 3rd trimester. Materials and Methods: We compared women participating in light-intensity (LI) stretching/breathing or no exercise (CON) across 24+ weeks of pregnancy Women with singleton pregnancies (<16 weeks), between 18-40 years, 18.5-34.99 kg/m2 BMI, and having no chronic health conditions were eligible. LI did 150 minutes light-intensity weekly exercise; CON did normal daily activities, but no exercise. Maternal measures included resting heart rate (HR) and blood pressure (BP). Fetal measures included estimated fetal weight (EFW), ponderal index (PI), HR, along with right and left ventricular measures (e.g., stroke volume, cardiac output, ejection fraction) at 36 weeks’ gestation. T-tests compared differences between groups; partial spearman rank correlations and regressions were performed to find relationships and predict fetal echocardiographic outcomes, controlling for fetal activity state. Results: Of 50 pregnant women (n=26 in LI, n=24 in CON), we found maternal exercise intensity influences fetal left ventricular heart flow, while maternal exercise duration influences fetal right ventricular outcomes. There were no differences (p>0.05) in fetal cardiac anatomical measures. Lastly, light intensity exercise and duration of exercise lower maternal blood pressure in late pregnancy. Conclusions:Light-intensity exercise is associated with improved fetal cardiac measures. Women benefit from light intensity exercise during pregnancy. Cardiovascular benefits from exercise for mother and child are dose dependent.

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.

Location of the placenta or the umbilical cord insertion site in the lowest uterine segment is associated with low maternal blood pressure

To evaluate whether placental abnormalities and umbilical cord insertion site affect the occurrence of pre-eclampsia and maternal blood pressure. Case-control study. Showa University Hospital, Tokyo, Japan. A total of 5722 consecutive women who delivered singleton infants were included in the study. The associations of placental abnormalities, the location of the placenta, the location of the cord insertion site, and maternal background with the occurrence of pre-eclampsia and maternal blood pressure at the term of pregnancy were analysed. Pre-eclampsia and maternal blood pressure at the term of pregnancy. Pre-eclampsia was observed in 236 women (4.1%). Pre-eclampsia was frequently observed in women with placental form abnormalities (odds ratio 3.0) and infarction of the placenta (odds ratio 5.3). Pre-eclampsia was observed in 0 and 4.1% of women with and without placenta praevia, respectively (P = 0.004), and in 0 and 2.5% of women with and without low cord insertion during the first trimester, respectively (P = 0.018). After adjustment for confounding variables, the multivariate regression analyses revealed reductions of 8.4 and 5.0 mmHg in systolic and diastolic blood pressure, respectively, in women with placenta praevia compared with women without placenta praevia, and reductions of 4.3 and 3.1 mmHg in systolic and diastolic blood pressure, respectively, in women with low cord insertion during the first trimester compared with women without low cord insertion. Not only placenta praevia but also low cord insertion are associated with low frequencies of pre-eclampsia and low maternal blood pressure.

Aldosterone, maternal volume status and healthy pregnancies: a cycle of differing views

In this month’s issue, Escher et al. [1] suggest that high aldosterone availability during pregnancy, measured as urinary tetra-aldosterone excretion, is associated with lower maternal blood pressure and larger, healthier neonates. The findings are preliminary with more studies required to confirm these authors’ suggestions, but of interest is that these data extend recent observations by this same group that recall past passionate debates concerning the volume status of normal gravidas and those developing preeclampsia. Also, the roles of the renin–angiotensin–aldosterone system (RAS), previously given short-shrift in discussions concerning preeclampsia’s pathogenesis and pathophysiology, have been resurrected by Escher et al.’s current observations and their previous publications, as well [1–4]. All agree that normal pregnancy is characterized by an absolute increment in both extracellular and intravascular volume (by some 6–7 L, at that), but investigators disagree on the meaning of these changes. For some (‘under-fill’ theory) it is an incomplete response to both the systemic vasodilation and markedly increased arterial global compliance characteristic of normal pregnancy, and indeed, the lower blood pressure and markedly stimulated RAS and aldosterone levels that persist during normal pregnancy are consistent with this paradigm. For others, this is an absolute hypervolaemia perhaps due to the higher levels of salt-retaining steroids that accompany gestation (‘overfill’ theory), and to still others, there is a constant resetting of the ‘volumestat’ as pregnancy progresses (‘normal-fill’ theory), the gravida always acting as if her current volume status were ‘normal’. There are data to support each view, detailed elsewhere [5,6], but the formulation popular with the authors of this commentary is that the observed physiologic changes characteristic of normal pregnancy, e.g. vasodilation, low normal blood pressure, increased cardiac output and activated RAS that responds normally to new volume challenges (e.g. salt loading or restrictions), appears consistent with the following formulation. There is an initial primary ‘under-filling’ very early in gestation, with rapid refilling, after which the gravida ‘senses’ her volume status as euvolaemia or ‘normal-fill’ throughout the remainder of her pregnancy [5,6]. There is a need to prove which of these theories of how pregnant women ‘sense’ their volumes is correct, as this should have relevance to designing the appropriate therapeutic approaches. The article of Escher et al. [1] by linking aldosterone availability to larger neonates and better pregnancy outcomes also recalls an older literature whose authors stressed that the magnitude of the increased plasma volume in pregnancy correlated with better fetal outcomes (reviewed in [7,8]). The rest of this commentary focuses on the volume status of preeclamptics and the status of the RAS in this disease. One of the most striking features of normal pregnancy, apparent both by physical examination and by haemodynamic and hormonal measurement, is early and marked vasodilation. The physiologic consequences—greater blood flow to the uteroplacental unit, increased renal blood flow and glomerular filtration rate, lower maternal blood pressure and increased cardiac output—are important accommodations to the growing fetus. Lower serum creatinine concentrations and increased plasma renin and aldosterone levels are some of the laboratory measures generally expected to accompany such physiological adaptations. In preeclampsia, characterized by hypertension and proteinuria after midgestation, the RAS is actually suppressed compared to women with uneventful gestations [5–7], although in most women, plasma renin activity and aldosterone levels are still considerably higher than in those with the non-pregnant state. The RAS is also suppressed in women with chronic hypertension who develop superimposed preeclampsia compared to hypertensive women who do not [9]. This suppression of the RAS occurs despite the fact that plasma volume, increased by ∼1.2 L in normal pregnancy, is lower in preeclampsia, the lowest values observed in women progressing to the convulsive phase of the disease eclampsia [6,10]. Again, and akin to differing interpretations given of the volume changes in normal

High aldosterone-to-renin variants of CYP11B2 and pregnancy outcome

Increased aldosterone concentrations and volume expansion of normal pregnancies are hallmarks of normal pregnancies and blunted in pre-eclampsia. Accordingly, we hypothesized an active mineralocorticoid system to protect from pre-eclampsia. In pregnant women (normotensive n = 44; pre-eclamptic n = 48), blood pressure, urinary tetrahydro-aldosterone excretion and activating polymorphisms (SF-1 site and intron 2) of the aldosterone synthase gene (CYP11B2) were determined; 185 non-pregnant normotensive individuals served as control. Amino acid-changing polymorphisms of the DNA- and agonist-binding regions of the mineralocorticoid receptor were evaluated by RT-PCR, SSCP and sequencing. Urinary tetrahydro-aldosterone excretion was reduced in pre-eclampsia as compared to normal pregnancy (P < 0.05). It inversely correlated with blood pressure (r = 0.99, P < 0.04). Homozygosity for activating CYP11B2 polymorphisms was preferably present in normotensive as compared to pre-eclamptic pregnancies, identified (intron 2, P = 0.005; SF-1 site, P = 0.016). Two mutant haplotypes decreased the risk of developing pre-eclampsia (RR 0.16; CI 0.05-0.54; P < 0.001). In contrast, intron 2 wild type predisposed to pre-eclampsia (P < 0.0015). No functional mineralocorticoid receptor mutant has been observed. High aldosterone availability is associated with lower maternal blood pressure. In line with this observation, gain-of-function variants of the CYP11B2 reduce the risk of developing pre-eclampsia. Mutants of the mineralocorticoid receptor cannot explain the frequent syndrome of pre-eclampsia.

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.

Does Low Maternal Blood Pressure During Pregnancy Increase the Risk of Perinatal Death?

A recent report described an association between low maximum diastolic blood pressure (DBP) during pregnancy and perinatal death (stillbirth and death in the first week combined). The authors did not account for gestational length, a strong predictor of perinatal death. We studied 41,089 singleton pregnancies from the U.S. Collaborative Perinatal Project (1959-1966). We observed an association between low maximum DBP and elevated risk of perinatal death. However, this association disappeared after accounting for reverse causation related to gestational length. At any given gestational week, women whose offspring ultimately experienced perinatal death did not have significantly lower maximum DBP than women whose offspring survived the perinatal period. When accounting for the trend of increasing DBP during late pregnancy through gestational-age-specific DBP standardized score, we saw no association between low diastolic blood pressure and perinatal death. Low maximum maternal DBP during pregnancy is a post hoc correlate of perinatal death, not a true risk factor.

Late decelerations and brain tolerance of the fetal monkey to intrapartum asphyxia

Eight monkey fetuses near term were subjected to regulated asphyxia during labor by mechanically constricting the maternal abdominal aorta and diminishing blood flow to the uterus. A magnitude of asphyxia was produced and maintained for an initial three hours that was close to but not sufficient to elicit late decelerations. The asphyxia was then augmented during a fourth hour to cause late decelerations of magnitudes of 5 to 15 per cent of the initial heart rate. After termination of the fourth hour of asphyxia, the fetuses were delivered by hysterotomy and provided intensive care. During the three to nine months of survival after birth, all animals were neurologically intact; on necropsy the brains were free of pathologic changes both grossly and microscopically. These results support the thesis that fetal heart rate monitoring during labor exhibits a sensitivity sufficient to diagnose asphyxia of the fetus of clinical significance before it reaches a magnitude that may cause permanent neurological injury. These results are particularty pertinent to those clinical circumstances where the decreases in intervillous space blood flow brought about by uterine contractions are accentuated due to low maternal blood pressure.

Formation of fetal cotyledons in the hemochorial placenta: A theoretical consideration of the functional implications of such an arrangement

The principal stages of organogenesis of the hemochorial placenta are known in a descriptive sense. These are recognized, after implantation, as previllous, villous, and cotyledonary. The previllous stage is first without maternal blood but shortly, uterine veins, and later endometrial capillaries, are tapped and lakes of maternal blood and products of fetal tissue breakdown form embryotrophe in the syncytium. This material is believed to be a source of nourishment for embryonic tissues. When the conceptus becomes surrounded by an abundance of villi of cytotrophoblastic columns that give rise continuously to a covering layer of syncytial tissue, this is called the chorion frondosum. It has been seen as late as 45 days conception age in a human conceptus. No one knows now the nature (arterial, venous) of maternal blood flow about these early fetal tissues. However, by the eighty-fourth day, definitive hollow tambour-like fetal cotyledons exist and these become larger, in these dimensions, as gestation continues. To account for the transformation of chorion frondosum into fetal cotyledons (40 to 60 cotyledons altogether, and about 150 undeveloped rudimentary ones that are residual anchoring villi with numerous free villi from the chorion frondosum) the view is advanced in this essay that when endometrial spiral arterioles are tapped (sometime after the fortieth day) the local force of blood pressure causes organization of the local fetal cotyledons, and that this is essentially a hemodynamic molding process acting on the tissues of the chorion frondosum. It involves (a) cavitation, (b) crowning and extension of anchoring villi, and (c) completion by development of the supplying vascular pattern out of the original blastoderm, now the chorioallantoic plate. Physiologic data from the literature (local blood pressure differences and oxygen tension differences within the intervillous space and cineangiography) are cited to support this functional concept of the last stages of definitive morphogenesis of the placenta.This theory raises questions concerning what metabolic factors limit trophoblastic invasiveness. It offers a solution by which physiologists may account for hydrostatic forces of a conventional sort in maternal-fetal exchange of water and many dissolved substances since the cotyledons are local regions of high maternal blood pressure with respect to fetal blood pressure, and the non-cotyledonary anchoring villi are areas of low maternal blood pressure with respect to fetal blood pressure. Each cotyledon is a terminal arterial glomus from which blood filters slowly through the surrounding fetal villi into the intervillous space proper. Without such a concept one is confronted with the currently prevailing view of uptake of water by fetal blood into capillaries where pressure is high (15 mm. Hg or more) from regions where the pressure is commonly regarded as being low (intervillous space, 5 to 10 mm. Hg).