SRI Supplement to Reproductive Sciences - Volume 25 Number 1 - March 2018 - 294A

294A

Reproductive Sciences Vol. 25, Supplement 1, March 2018

CONCLUSION: VTE is a significant cause of morbidly and mortality
in pregnancy and the puerperium, both in the developed and developing
world. Risk factors such as parity, lupus and high BMI should be identified
and scored accordingly. Prophylactic thromboprophylaxis should
commence as per local guideline. Early Identification and individualized
risk assessment of high-risk patients is crucial for VTE prevention and
treatment.

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Association between Longitudinal Lifelog and Preterm Birth in
Maternity Log Study. Daisuke Ochi,1,2 Takafumi Yamauchi,1,2 Yoshiki
Tsunemoto,1 Maiko Wagata†,2 Riu Yamashita,2 Yuki Harada,2 Osamu
Tanabe,2 Nobuo Yaegashi,3 Satoshi Hiyama,1 Masao Nagasaki,2 Junichi
Sugawara*.2 1NTT DOCOMO, Inc., Yokosuka, Kanagawa, Japan; 2Tohoku
University, Sendai, Miyagi, Japan; 3Tohoku University Graduate School
of Medicine, Sendai, Miyagi, Japan.
INTRODUCTION: Pregnancy related disorders, including preterm birth
(PTB), are caused by a complex interaction of genetic and environmental
factors such as lifestyle and living environment. We have designed a
prospective cohort study named "Maternity Log Study" to investigate
unrevealed mechanisms of those disorders from both genetic and
environmental aspects.
METHODS: A total of 302 participants were recruited by written
informed consent. We collected daily lifelogs of physiological data (body
weight, blood pressure, pulse rate, physical activity, body temperature, and
hours of sleep) and symptoms (morning sickness, abdominal pain, uterine
contraction, and bowel movement) as well as blood and urine samples at
several points throughout pregnancy. We analyzed the association between
the course of lifelogs and PTB.
RESULTS: Several lifelog features showed differences between a
spontaneous PTB (SPTB) group (n=14) and a control group (n=77).
Especially, daily caloric expenditure of the SPTB group measured by a
wearable activity monitor was significantly lower than controls after 20
weeks of gestation (1655±221 vs 1949±297 kcal, p<0.002). An adjusted
odds ratio of daily caloric expenditure was 0.61 (95%CI 0.43 to 0.83) at
20 weeks of gestation. Interestingly, morning body temperatures of the
control group decreased gradually according to the gestational age (36.56
-> 36.36°C from 16 to 30 weeks of gestation), while those of the SPTB
group did not as much (36.64 -> 36.54°C during the same period as the
control). An adjusted odds ratio of morning body temperatures was 0.50
(95%CI 0.38 to 0.66) at 20 weeks of gestation. A SPTB prediction model
using lifelogs before 26 weeks of gestation demonstrated sensitivity higher
than 0.85 and specificity higher than 0.90.
CONCLUSION: Combinations of daily lifelogs could be predictive
markers for SPTB. Further combinations with genome, transcriptome,
and metabolome data may improve our prediction model and reveal
underlying mechanisms of SPTB.

S-127
First Trimester Changes in Arterial Stiffness and Risk of Subsequent
Hypertension in Pregnancy. Erin A Morris, Carole A McBride, Gary J
Badger, Ira M Bernstein*. University of Vermont College of Medicine,
Burlington, VT, United States.
INTRODUCTION: Evidence exists that increased arterial stiffness,
when examined either prior to or during pregnancy, is associated with the
development of hypertensive disorders of pregnancy. We aimed to examine
the influence of pregnancy on arterial stiffness in different vascular beds.
We hypothesized that women who develop hypertension in pregnancy
(HTN) would show evidence of increased arterial stiffness both prior to
pregnancy and in the first trimester.
METHODS: This is a secondary analysis of a larger prospective
observational study. Women underwent detailed cardiovascular
assessment prior to planned pregnancy and returned for a second
cardiovascular assessment between 10 and 14 weeks gestation. Pulse wave
velocity (PWV) was determined from pulse wave forms obtained with
Doppler ultrasound as time from EKG R wave to initial systolic flow in the
brachial artery (brachial PWV) and in the popliteal artery (aorto-femoral
PWV). Birth outcomes were obtained via chart review. Group differences

Scientific Abstracts

were assessed by Student's t-test to determine the associations between
pre-pregnancy and first trimester PWV in the brachial and aorto-femoral
regions with subsequent HTN.
RESULTS: 65 women underwent cardiovascular assessment prior to
pregnancy (v1), subsequently conceived singleton pregnancies, and
returned for a first trimester cardiovascular assessment (v2). The mean
age of participants was 30.6 ± 4.2 years, with mean BMI of 25.5 ± 6.3
kg/m2. 47 women (72%) were nulliparous at study entry. 18 (28%)
had a history of preterm preeclampsia in a prior pregnancy. Prior to
pregnancy, all women were studied in the luteal phase. V2 occurred at a
mean gestational age of 12.9 ± 0.8 weeks. All women delivered liveborn
infants. 12 women developed preeclampsia and 11 were diagnosed with
gestational hypertension according to ACOG diagnostic criteria. PWV
measured at v1 was not significantly associated with subsequent HTN,
although women who developed HTN tended to have faster PWV in the
brachial region than did controls at v1 (p = .08). In the first trimester,
women who developed HTN had faster PWV in both the brachial (HTN
= 8.67 ± 2.48 m/s, CTL = 7.42 ± 1.27 m/s, p = .032) and aorto-femoral
regions (HTN = 4.02 ± 0.50 m/s, CTL = 3.73 ± 0.45 m/s, p = .022). PWV
did not change significantly in either region between v1 and v2 for women
who developed HTN (+0.24 ± 2.7 m/s and +0.14 ± 0.60 m/s respectively)
or for controls (-0.30 ± 1.78 m/s and -0.03 ± 0.48 m/s respectively).
CONCLUSION: We found that women who develop HTN in pregnancy
show evidence of increased arterial stiffness prior to pregnancy that is
further amplified in the first trimester, likely as a result of inadequate
arterial remodeling. This subclinical vascular pathology may predispose
women to both hypertension in pregnancy and long-term cardiovascular
morbidity.

S-128
Estrogen-Responsive Uterine Artery Blood Flow is Dependent on
Cystathionine γ Lyase (CSE). Rachael Bok, Sara A Wennersten, K
Joseph Hurt*. University of Colorado School of Medicine, Aurora, CO,
United States.
INTRODUCTION: Pregnancy induces a dramatic rise in uterine blood
flow (UBF), which is mediated by estrogen (E2)-dependent stimulation
of uterine artery nitric oxide (NO) production. Inadequate UBF increases
the risk for fetal growth restriction and preeclampsia. CSE enzymatically
produces the small molecule gasotransmitter hydrogen sulfide (H2S),
which can be a co-mediator with NO for some vascular function. In this
study, we assessed the role of CSE in E2-stimulated UBF using a CSE
knockout (CSE KO) mouse model.
METHODS: Virgin C57/BL6 wild type (WT) or CSE KO mice (3-4
months) were ovariectomized and recovered for two weeks. Mice were
anesthetized with isoflurane in O2 and body temperature maintained
by ambient warmer, and UBF was assessed by transcutaneous microultrasound (VisualSonics). Doppler waveforms were obtained using color
flow mapping from the left uterine artery (UA) near the internal iliac
artery at baseline and after two days of hormone injection (sesame oil
vehicle or 0.5 mg/kg/day E2). Velocity and diameter were averaged from
three consecutive cardiac cycles and corrected for color Doppler artifact.
Parabolic blood flow velocity distribution was assumed, and flow (mL/
min) was calculated by Q=½πPV(D/2)2 and normalized to body weight
(kg). Total serum NO metabolites (NOx = NO2- plus NO3-) were measured
using a Total Nitric Oxide assay. Results are reported as mean ± SEM
where n refers number of animals. p<0.05 was considered significant.
RESULTS: UBF (mL/min-kg) for WT and CSE KO was similar at
baseline (16.5 ± 1.3, n=21 vs. 15.8 ± 1.9, n=23) and after vehicle treatment
(17.7 ± 3.4, n=5 vs 14.0 ± 1.3, n=8). E2 increased UBF by 91% in WT (n=8,
p<0.01), but had no significant effect on UBF in CSE KO (10% increase,
n=5). Renal artery blood flow was not different between strains at baseline
(35.5 ± 4.0, n=23 WT vs. 27.4 ± 3.9 CSE KO), and was unaffected by
vehicle or E2 treatment. Total serum NOx was similar in WT and CSE KO
with vehicle treatment, but significantly reduced in E2-treated CSE KO
mice vs. WT (15.8 ± 1.2 μM, vs. 25.9 ± 2.5 μM; p<0.01).
CONCLUSION: Diminished E2-stimulated UBF in CSE KO mice
suggests that CSE and H2S may regulate UBF in pregnancy. Decreased
NOx with E2 in CSE KO mice suggests altered endothelial nitric oxide

Table of Contents for the Digital Edition of SRI Supplement to Reproductive Sciences - Volume 25 Number 1 - March 2018