Preeclampsia and fetal growth restriction during pregnancy are associated with increased risk of maternal cardiovascular disease later in life. It is unclear whether this association is causal or driven by similar antecedent risk factors. Clarification requires recruitment before conception which is methodologically difficult with high attrition rates and loss of outcome numbers to nonconception/miscarriage. Few prospective studies have, therefore, been adequately powered to address these questions. We recruited 530 healthy women (mean age: 35.0 years) intending to conceive and assessed cardiac output, cardiac index, stroke volume, total peripheral resistance, mean arterial pressure, and heart rate before pregnancy. Participants were followed to completion of subsequent pregnancy with repeat longitudinal assessments. Of 356 spontaneously conceived pregnancies, 15 (4.2%) were affected by preeclampsia and fetal growth restriction. Women who subsequently developed preeclampsia/fetal growth restriction had lower preconception cardiac output (4.9 versus 5.8 L/min; P =0.002) and cardiac index (2.9 versus 3.3 L/min per meter 2 ; P =0.031) while mean arterial pressure (87.1 versus 82.3 mm Hg; P =0.05) and total peripheral resistance (1396.4 versus 1156.1 dynes sec cm − 5 ; P <0.001) were higher. Longitudinal trajectories for cardiac output and total peripheral resistance were similar between affected and healthy pregnancies, but the former group showed a more exaggerated fall in mean arterial pressure in the first trimester, followed by a steeper rise and a steeper fall to postpartum values. Significant relationships were observed between cardiac output, total peripheral resistance, and mean arterial pressure and gestational epoch. We conclude that in healthy women, an altered prepregnancy hemodynamic phenotype is associated with the subsequent development of preeclampsia/fetal growth restriction.

OBJECTIVE:Birth weight (BW) is thought to be determined by maternal health and genetic, nutritional and placental factors, the latter being influenced by anatomical development and perfusion. Maternal cardiovascular changes contribute to uteroplacental perfusion; however, they have not yet been investigated in relation to fetal growth or BW. Our aim was to explore the relationship between maternal cardiovascular adaptation, fetal growth and BW in healthy pregnancies. METHODS:This was a longitudinal prospective study of women planning to conceive a pregnancy. Maternal cardiac output (CO), cardiac index (CI), pulse-wave velocity, aortic augmentation index, central blood pressure and peripheral vascular resistance were assessed prior to pregnancy and at 6, 23 and 33 weeks' gestation. Fetal growth was assessed using serial ultrasound measurements of biometry. RESULTS:In total, 143 women volunteered to participate and were eligible for study inclusion. A total of 101 women conceived within 18 months and there were 64 live births with normal pregnancy outcome. There were positive correlations between BW and the pregnancy-induced changes in CO (ρ = 0.4, P = 0.004), CI (ρ = 0.3, P = 0.02) and peripheral vascular resistance (ρ = 0.3, P = 0.02). There were significant associations between second-to-third-trimester fetal weight gain and the prepregnancy-to-second-trimester increase in CO (Δ, 0.8 ± 1.2 L/min; ρ = 0.3, P = 0.02) and CI (Δ, 0.4 ± 0.6 L/min/m2 ; ρ = 0.3, P = 0.04) and reduction in aortic augmentation index (Δ, -10 ± 9%; ρ = -0.3, P = 0.04). CONCLUSIONS:In healthy pregnancy, incremental changes in maternal CO in early pregnancy are associated with third-trimester fetal growth and BW. It is plausible that this association is causative as the changes predate third-trimester fetal growth and eventual BW. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

STUDY QUESTIONAre there differences in preconception cardiovascular function between women who have a viable pregnancy and those who have a first trimester miscarriage?SUMMARY ANSWERPreconception cardiovascular function of central haemodynamics and arterial function are similar between women who have a viable pregnancy and those who have a first trimester miscarriage.WHAT IS KNOWN ALREADYMiscarriages have been associated with increased long-term cardiovascular disease risk, and arterial and cardiovascular dysfunction has been hypothesised as the common link. It is not known if these risks are present prior to pregnancy or are a reflection of poor arterial and haemodynamic adaptation to pregnancy.STUDY DESIGN, SIZE, DURATIONThis prospective longitudinal preconception cohort study was conducted over 18 months. In total, 367 participants were recruited pre-pregnancy, from which 197 pregnancies were recorded; 39 of these pregnancies ended in first trimester miscarriage. Complete longitudinal data were available for 172 pregnancies (140 viable pregnancies, 32 first trimester miscarriages) from pre-pregnancy to 6 weeks gestation.PARTICIPANTS/MATERIALS, SETTING, METHODSThis was a single site study based at a maternity hospital in London. Healthy women were recruited prior to natural conception and followed up once they became pregnant. All underwent haemodynamic [cardiac output (CO), peripheral vascular resistance (PVR)] and arterial function [aortic augmentation index (AIx) and pulse wave velocity (PWV)] testing prior to pregnancy and at 6 weeks gestation, using non-invasive devices (gas re-breathing method, Innocor® and an occilometric device, Vicorder®). Cross-sectional measurements at pre-pregnancy and 6 weeks gestation and a longitudinal analysis of changes were compared between women who had a subsequent viable pregnancy, and those who had a subsequent first trimester miscarriage.MAIN RESULTS AND THE ROLE OF CHANCEThere were no differences between women destined to have a healthy ongoing pregnancy compared to those who miscarried, in terms of baseline cardiovascular function, assessed by CO, PVR, PWV or AIx. Similarly, between the groups, there were no differences in pregnancy adaptation with similar trends in cardiovascular function changes from pre-pregnancy to 6 weeks gestation.LIMITATIONS, REASONS FOR CAUTIONWhilst this is the first study to investigate preconception and early pregnancy haemodynamic and arterial function in relation to viability, the relatively modest number of miscarriages may not be sufficient to show subtle differences in haemodynamic changes if these were present.WIDER IMPLICATIONS OF THE FINDINGSThis study suggests that pre-pregnancy haemodynamic and arterial function is unlikely to be the causal link between miscarriages and future cardiovascular disease. Our findings suggests that factors other than the presence of a viable embryo drive cardiovascular changes in early pregnancy. This study raises new questions about miscarriages as an independent risk event which predisposes women to increased cardiovascular risk later in life.STUDY FUNDING/COMPETING INTEREST(S)The investigators are funded by NIHR Imperial BRC, NIHR Cambridge BRC, Action Medical Research, Imperial College Healthcare Charity and Tommy's Charity. We acknowledge the loan of ultrasound equipment from Samsung Medison (South Korea)/MIS Ltd and provision of fertility monitors from SPD Development Company Ltd (Bedford, UK). There are no competing interests. C.C.L. is supported by the UK National Institute for Health Research Biomedical Research Centre based at Imperial College Healthcare National Health Service Trust and Imperial College London.TRIAL REGISTRATION NUMBERN/A.

It is hypothesised that maternal cardiovascular (CV) dysfunction may be present prior to conception. With pregnancy, a decompensation of CV function may manifest as pre-eclampsia (PE) or fetal growth restriction (FGR). We hypothesise that pre-pregnancy (PP) exercise stress testing is comparable to gestation related physiological stress, and may relate to pregnancy outcome. To investigate this, we prospectively examined PP exercise stress test responses in healthy women planning to conceive, in association with subsequent pregnancy outcome, specifically PE/FGR. We recruited non-smokers with no CV comorbidities into a pre-conception study. All participants had non-invasive measurements of cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), heart rate (HR) and brachial blood pressure (BP) at rest. These tests were repeated during and after a 3-minute Dundee step test. Delta (δ) values were calculated between resting and subsequent exercise measurements to deduce exercise stress response. For data analysis, women who subsequently conceived a pregnancy affected by PE/FGR were assigned to ‘pathology’ group and those with unaffected pregnancies to a control group. Controls had significantly higher CO (mean CO 10.14 vs 8.76 L/min, p= 0.042) and SV(p=0.016) compared to the pathology group. δTPR between the groups was also statistically different(p=0.007). PE/FGR group have greater peak HR and delta HR values (peak HR[control =99.56 bpm, pathology =111/33bpm, P=0.002] and δHR response [control mean=17.87 bpm, pathology mean=26.72 bpm P=0.032]). We report differences in cardiovascular response to stress between women who subsequently conceive a pregnancy affected by PE/FGR and those with normal pregnancy outcome. Normal stress response is increased CO and reduced TPR. CO increments by increasing SV was more pronounced in controls, whereas the pathology group had more pronounced HR increase.

To understand the reproductive health of a population, it is important to account for all conceptions and spontaneous pregnancy loss. Reported rates with spontaneous conceptions are conflicting. We conducted a prospective pre-conception study of women planning a pregnancy, to examine per-cycle conception and miscarriage, including early pregnancy loss (EPL) rates. Healthy women who were planning to conceive naturally were recruited into a pre-conception study. With an ovulation and pregnancy testing monitor, subjects commenced ovulation testing from cycle day 6 till LH surge was detected. Pregnancy testing commenced 7 days post-ovulation till a positive pregnancy result, or next menses. Monitor digital data was downloaded, providing semi-quantitative levels of LH and HCG. The interval between ovulation and a first rise in HCG baseline taken to represent implantation (O-I), and trend of rise in hCG, were related to pregnancy outcome (viable or miscarriage). Of 387 women recruited, 293 pregnancies were conceived, with per-cycle conception rate of 34.2% and interval to conception of 3.1 months. 87 pregnancies ended in 1st trimester miscarriages. 41% of miscarriages were ‘biochemical’ losses which would otherwise be clinically unrecognised. There were significant differences in O-I interval mean distance to median (p <0.001), and in hCG signal form as early as 1 day of rise in baseline (p <0.0001), between pregnancies that miscarried, and viable pregnancies. Spontaneous pregnancy per-cycle conception rate is 34.2% with pregnancy loss rate of 30%, higher than that previously reported in the literature, as EPL were also accounted for. A vast number of pregnancies are lost prior to the window of ultrasound-diagnostic miscarriage criteria. Both short and long O-I interval, and different b-hCG rise from very early stages is associated with miscarriage.

Several studies have compared cross-sectional non-invasive techniques for the measurement of cardiac output (CO) in pregnant women, but studies with longitudinal design are lacking. We aimed to compare the ability of two devices, Vicorder® and Innocor®, in tracking changes in CO from pre-pregnancy to post-partum in healthy women. Innocor has previously been validated against invasive techniques but not Vicorder. Non-smoking women, between 18-44 years, with BMI <35 were selected from a prospective ongoing study (CONCEIVE) on cardiovascular function from prior to pregnancy to post-partum 2014-2017. For data analysis, only healthy pregnancies were included. Measurements were obtained using Vicorder first, and then Innocor under standardised conditions, and repeated at 6 time points (non-pregnant, 6, 10, 22, and 34 weeks gestation, and post-partum). The difference in CO values obtained between time points (ΔCO) were calculated (15 ΔCO per participant for each device). We used a four-quadrant plot with exclusion zone of 0.5 L/min and calculated concordance rate, angular bias and radial limits of agreement (LOA). A concordance rate of 85% was considered acceptable. By using a linear mixed model analysis we tested whether the longitudinal change in CO differs between the two devices. 69 participants were included (1035 measurements). The concordance rate was 64%, angular bias 0.6836 and radial LOA 12.87-77.13. The longitudinal trajectory of CO recorded with the two devices differed significantly (p=0.0093). The maximum rise in CO happened in the late 1st-beginning of 2nd trimester, however with Innocor it increased by 15% compared to pre-pregnancy values and with Innocor by 7% only. Despite low angular bias, a low concordance rate suggests that the agreement between devices is poor; therefore, they shouldn't be used interchangeably within the same subject through pregnancy. Interestingly, the increase in CO from prior to pregnancy with both devices appears more modest than previously reported.

1. Division of Cancer & Surgery, Imperial College London, Institute for Reproductive & Developmental Biology, Du Cane Road, London, W12 0HS. 2. Division of Experimental Medicine & Immunotherapeutics, University of Cambridge, ACCI, Addenbrookes Hospital, Hills Road, Cambridge, CB2 0QQ. 3. St George’s, University of London & St George’s University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute. London, SW17 0RE

There is strong evidence supporting the role of maternal arterial dysfunction in pregnancy‐specific disorders such as pre‐eclampsia and intrauterine growth restriction. As more work is focused towards this field, it is important that methods and interpretation of arterial function assessment are applied appropriately. Here, we summarize techniques and devices commonly used in maternal health studies, with consideration of their technical application in pregnant cohorts. Copyright © 2017 ISUOG. Published by John Wiley & Sons Ltd.

Cardiac output (CO) is a key investigation in hemodynamic research. Invasive techniques are not appropriate in healthy pregnant women and non-invasive devices are widely used, although few have been tested in pregnancy. We performed a cross-sectional comparison of CO measurements from two non-invasive devices: Innocor®, an inert gas re-breathing device validated against thermodilution and direct Fick method, and Vicorder®, a new oscillometric- based device, in non-pregnant and pregnant healthy women. Non-smoking women, aged 18-44 years, with Body Mass Index <35 were selected from two prospective ongoing studies (CONCEIVE and PRECEPT) with identical protocol for CO measurements. Participant visits ranged from pre-pregnancy to post-partum, and only those with normal pregnancy outcome were selected for data analysis. Measurements of CO were made using Vicorder first, and then Innocor, and divided into 6 bands (non-pregnant, early first, late first, second, third trimester and post-natal). Bland Altman and intraclass correlation coefficient (ICC) analysis was performed. A low bias indicating accuracy, narrow limits of agreement (LOA) with percentage error <30% reflecting precision was considered to reflect good agreement (Critchley's criteria). In total, from 413 participants, 1141 CO measurements from each device were obtained. For the whole population, the bias between single measurements was 0.23 l/min, standard deviation of bias 1.48 l/min, LOA 3.36-9.18, percentage of error 46% and ICC of 0.348. Similar results were obtained when each time point was analysed separately. Despite low bias (mean difference in CO), the LOA are wide, percentage of error is above 30% and ICC is low, indicating that there is poor agreement between both devices for individual CO measurements. Before these devices can be applied in a clinical setting, further validation against a gold standard is required, though this may not be possible in healthy obstetric cohorts.

It is suggested that maternal cardiovascular(CV) changes in pregnancy are related to pregnancy outcome, specifically failure of these important adaptive changes may result in pre-eclampsia(PE) or fetal growth restriction (FGR). To explore if maternal physiological CV maladaptation could be anticipated prior to pregnancy, we investigated pre-pregnancy (PP) exercise stress testing prior to conception, in association with subsequent pregnancy induced CV changes. We recruited non-smokers with no CV co-morbidities into a pre-conception study. PP, all participants had non-invasive measurements of cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), heart rate (HR) and brachial blood pressure (BP) at rest. These were repeated during and after a 3-minute Dundee step test. Delta (δ) values were calculated between resting and exercise measurements to deduce exercise stress response. At 22 weeks' gestation resting CV measurements were repeated. Delta values induced by exercise PP were related to longitudinal changes induced by pregnancy (PP to 22wks). There were significant correlations between PP exercise induced CV changes, and PP to 22 weeks induced CV changes for CO, HR, BP and TPR. The strongest correlation was between the PP δTPR during exercise & the pregnancy induced adaptation of TPR from PP to 22 wks (r=0.669, p<0.001.) We explored if the δTPR relationship was also present at 6 weeks gestation and found similar results, though with weaker correlations (r=0.568, P<0.001). TPR exercise response strongly correlates to physiological change in TPR from PP to mid-pregnancy (22wks). This correlation is already present by 6 wks gestation, though to a weaker extent. There are also weaker but significant associations between PP exercise CO, BP and mid-pregnancy adaptation of the same parameters. Therefore, PP exercise testing may be valuable in providing insight into normal physiological adaptation to pregnancy.

Women affected by PE/IUGR are noted to have a higher risk of cardiovascular (CV) disease later in life. It is hypothesised that subtle perturbations in maternal CV function might be present prior to conception, which pre-disposes women to PE/IUGR due to increasing physiological strain of pregnancy, and CV disease late in life due to age related changes. To investigate this, we conducted a prospective pre-conception study of healthy women planning a pregnancy, to examine the relationship between pre-conception CV parameters and conception of a pregnancy complicated by PE /IUGR. 527 healthy women (BMI < 35, non-smokers with no cardiovascular co-morbidities) planning to conceive naturally were recruited. All had non-invasive measurements of cardiac output (CO), peripheral and central blood pressure (BP), systemic vascular resistance (PVR), arterial stiffness and exercise testing prior to pregnancy and once pregnant, longitudinal repeat measurements every trimester until postpartum. 218 women conceived a pregnancy which resulted in a live birth within study timeline, of which 14 had a pregnancy affected by PE or IUGR. Interval between pre-conception CV measurements and conception was 3.9 months. Adjusting for BMI, parity and age, women who developed PE/IUGR had significantly lower pre-conception CO (5.8 ± 1.0 vs. 5.0 ± 0.6 L/min; p = 0.007), and higher PVR (Mann-Whitney mean rank 105 vs. 167; p <0.001) and BP (p =0.026) compared to those with healthy pregnancy. Stress exercise testing revealed significantly different responses in terms of increments in stroke volume (p=0.02) and heart rate (p=0.04) between groups. In healthy women, significantly different central hemodynamic patterns and stress responses prior to conception, are associated with subsequent development of PE/IUGR. This raises questions on the origin aetiology point for these disorders, largely thought to arise from defective placentation in the first trimester.

Pregnancy has been likened to a stress test on the body, heart and circulation system. We hypothesise that pre-pregnancy (PP) exercise stress testing is comparable to gestation related physiological stress, and may relate to final outcome such as birthweight. To investigate this, we prospectively examined PP exercise stress test responses in healthy women planning to conceive, in association with gestation adjusted birthweight z-score. We recruited healthy non-smokers with no CV comorbidities into a pre-conception study. All participants had non-invasive measurements of cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), heart rate (HR) and brachial blood pressure (BP) at rest prior to pregnancy. These tests were repeated during and after a 3-minute Dundee step test. Delta(δ) values were calculated between resting measurements and subsequent exercise measurements to deduce exercise stress response. Birth weights were obtained from medical records and adjusted for gestational age (birthweight Z scores), which were analysed alongside pre-pregnancy CV measurements. Significant though weak correlations were observed between birth weight z-score and CO (R=0.228, p=0.006 [2side]), SV (R=0.221, P=0.009), TPR (R=-0.0189, p=0.025), and δTPR (R=0.181, p=0.032). We report that stress exercise induced changes in CO, SV and TPR prior to conception are related to birthweight Z scores in subsequent pregnancy, with positive correlations in CO, SV and dTPR a negative correlation of TPR. Therefore, women with greater exercise responses in CO, SV and TPR may be more likely to conceive larger babies.

Studies in pre-eclampsia have demonstrated that central hemodynamic changes give more insight than peripheral measures into maternal cardiac and vascular physiology. This study aims to investigate augmentation index (AIX) and pulse wave velocity (PWV) in pregnancies affected by fetal growth restriction (FGR) and compare them to healthy women in the third trimester of pregnancy. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. PWV is widely used as measure of arterial stiffness and predictor of future cardiovascular risk outside pregnancy. 8 pregnancies with fetal growth restriction (AC<10th percentile and raised umbilical PI) in the third trimester (27–35 weeks gestation) were compared with 42 healthy pregnancies in similar gestation band. AIX and PWV were measured by the Vicorder device with women in the left lateral position. Unpaired t-test was used to calculate the p value amongst these groups. The mean AIX in pregnancies with FGR was 22.63 compared to 10.10 in healthy pregnancies (p = 0.0005). PWV was 8.15 in the FGR group compared to 7.08 in healthy controls (p = 0.004). Pregnancies affected by third trimester FGR in the absence of pre-eclampsia show impairment of arterial function. Characterisation of arterial profile could play an important role in the understanding of the etiology of this condition which has hitherto been ascribed purely to placental dysfunction.

Abstract Introduction: This pilot study aims to compare cardiac output (CO) and total peripheral resistance (TPR) in pregnancies with fetal growth restriction (FGR) with healthy normal third trimester of pregnancies. Most studies previously done on cardiac parameters in pregnancy focused mainly on pre-eclampsia (PE) and FGR with PE, but not in normotensive FGR women. Methods: Eight pregnancies with FGR (AC < 10th percentile with raised umbilical PI) in the third trimester (27–35 weeks gestation) compared with 42 uncomplicated ongoing pregnancies within similar gestation bands. CO was measured non-invasively using INNOCOR inert gas re-breathing technique, with the participant standing upright. TPR was measured by the Vicorder device with women in the left lateral position. Unpaired t-test is used to calculate the p values among these groups. Results: Mean CO in pregnancies with FGR was 4.99 l/min and 5.65 l/min in healthy pregnancies (p = 0.08). Mean TPR (dyn.s.cm−5) was 0.95 in FGR and 0.83 in healthy pregnancies (p = 0.05). See Charts. Conclusions: There is no significant difference in CO between the two groups but TPR is higher in fetal growth restriction. This would support the theory of a hypodynamic circulation affecting these pregnancies, suggesting maternal cardiovascular maladaptation. It is worth noting that the numbers of patients in this early work are still small; however, the general trend does reflect that of the finding of Valensise et al. [1]. We plan to determine CO and TPR in relation to both gestation of onset and clinical deterioration prompting delivery. By characterizing these cardiovascular changes and their timing might allow for future intervention to modify cardiovascular function and plan optimal time of delivery.

AbstractIntroduction: Inadequate cardiovascular adaptation to pregnancy has been postulated as a potential cause or consequence of early pregnancy loss. We sought to investigate pre- and early pregnancy cardiovascular function in women with a viable pregnancy beyond the first trimester, and those suffering a first trimester pregnancy loss.Methods: We recruited healthy women trying for pregnancy without assisted reproductive technology into an observational pre-conception study, and recorded pregnancy loss as a clinical endpoint. The participants underwent comprehensive cardiovascular testing, including assessments of cardiac output (CO) using a noninvasive gas rebreathing method in lying and standing position. CO values were adjusted for body surface area and reported as cardiac index (CIdx). Participants that conceived a pregnancy were assessed at 6 weeks gestation with repeat CO and CIdx measurements, and a fetal viability scan. We compared change (delta) in CO and CIdx between pre-pregnancy and 6 weeks...

Pregnancies lost prior to the point of which a clinical pregnancy can be diagnosed by ultrasound, usually prior to 6 weeks gestation, are described as chemical pregnancies. To accurately define rate of 1st trimester pregnancy losses, requires prospective follow-up of women from pre-conception, until the occurrence of pregnancy loss (PL). The rate of PL in previous pre-conception studies have been quoted as 31–32.9%. However, the gestation at which PL occurs has not previously been reported. We recruited healthy women trying for pregnancy without assisted reproductive technology into an observational pre-conception study, and recorded pregnancy loss as a clinical endpoint. Participants were provided with digital ovulation and pregnancy monitors (SPD Development Company Ltd) to track day of ovulation (first day of LH surge) and estimated day of embryonic implantation (first day of positive pregnancy test). Participants were instructed to contact the research team as soon as they saw a positive pregnancy result. They underwent ultrasound scan at 6 weeks gestation to confirm viability and pregnancy location. 292 participants were recruited, of which 149 women conceived a pregnancy. Some participants conceived more than two pregnancies during the course of the study; the total number of pregnancies conceived is 176. Of these pregnancies, 54 resulted in pregnancy loss, with gestation at loss (day of scan diagnosis or pregnancy test reverting from positive to negative) ranging from 3 + 1 to 12 + 2 weeks gestation (mean: 6 + 5 weeks), and 41% being before 6 weeks. The average interval ovulation-implantation for non-viable vs viable pregnancies is 11.45 and 12.88 days respectively. The average gestation of pregnancy loss in a healthy pre-conception cohort is 6 + 5 weeks, with almost one half being lost prior to 6 weeks.

Cardiovascular maladaptation to pregnancy has been postulated as a potential cause or consequence of early pregnancy loss. We investigated pre- and early pregnancy cardiovascular function in women with a viable pregnancy beyond the first trimester, and those with first trimester pregnancy loss. We recruited healthy women trying for pregnancy without assisted reproductive technology and recorded miscarriage as an outcome. Cardiac output (CO) and cardiac index (CIdx) were assessed using a gas rebreathing method in lying and standing postures. Participants who conceived were assessed at 6 weeks gestation with repeat CO/CIdx measurements and a viability scan. We compared change (delta) in CO and CIdx between pre-pregnancy and 6 weeks gestation between participants with sonographic diagnosis of pregnancy of unknown viability and subsequently miscarried (Group 1: 11 women), participants with normal scan at 6 weeks gestation but subsequently miscarried (Group 2: 17 women) and 25 matched controls who had normal 6 week scan and viable pregnancy beyond the first trimester. 176 pregnancies were conceived within 16 months. Fifty-four pregnancies miscarried in the first trimester, 26 before first scheduled post conception visit at 6 weeks. Six week cardiovascular and ultrasound data were available for the 28 women. There was no significant difference between delta lying CO (p = 0.3876, CI −1.733 to 0.733; p = 0.1781, CI −1.326 to 0.267) and CIdx (p = 0.3029, CI −0.767 to 0.627; p = 0.7615, CI −0.78 to 0.587) between the Group 1 and 2 respectively and controls, nor between delta standing CO (p = 0.2251, CI −0.56 to 2.219; p = 0.6137 CI −1.505 to 0.917) or CIdx (p- 0.4658 CI −0.364 to 1.146; p = 0.6349 CI −0.886 to 0.557). There is no difference in maternal cardiovascular adaptation in relation to pregnancy viability at 6 weeks in women who subsequently have a first trimester miscarriage, compared to healthy pregnancies. Changes in maternal cardiac output may be related more to the presence of trophoblast than to a viable embryo.

Introduction: Studies in pre-eclampsia have demonstrated that central haemodynamic changes give more insight than peripheral measures into maternal cardiac and vascular physiology. This study aims to investigate augmentation index (AIX) and pulse wave velocity (PWV) in pregnancies affected by fetal growth restriction (FGR) and compare them to healthy women in the third trimester of pregnancy. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. PWV is widely used as measure of arterial stiffness and predictor of future cardiovascular risk outside pregnancy.Methods: Eight pregnancies with fetal growth restriction (AC < 10th percentile and raised umbilical PI) in the third trimester (27–35 weeks gestation) were compared with 42 healthy pregnancies in similar gestation band. AIX and PWV were measured by the Vicorder device with women in the left lateral position. Unpaired t-test was used to calculate the p values amongst these groups.Results: The mean AIX in pregnancies with FGR was 22.63 compared to 10.10 in healthy pregnancies (p = 0.0005). PWV was 8.15 in the FGR group compared to 7.08 in healthy controls (p = 0.004). See charts.Conclusions: These results show that pregnancies affected by third trimester FGR in the absence of pre-eclampsia show impairment of maternal arterial function with high arterial stiffness. To date, many studies have shown impaired maternal arterial function in preeclampsia but little has been done to characterize maternal arterial function in fetal growth restriction alone. Considering both these conditions are thought to have common underlying etiology, these results suggest that arterial function is impaired in fetal growth restriction independent of hypertension or pre-eclampsia. Characterization of arterial profile could play an important role in the understanding of the etiology of this condition which has hitherto been ascribed purely to placental dysfunction.