Results
A total of 46 women were enrolled. Six patients were excluded due to:
Delivery at another institution (2), withdrawn consent (2), technical
difficulties with echo (1) non-reassuring fetal heart tones (1), leaving
40 patients for final analysis. The 40 women studied were distributed
into the 4 groups as follows: early PEC (N=10) matched early controls
(N=11), late PEC (N=9) and matched late controls (N=10). Women with
multiple gestations were excluded from the study. Demographic and
clinical characteristics of the study groups are presented in Table 1.
Mean maternal age and the incidence of smoking were not different across
the four groups. The incidences of diabetes in the late PEC group and
was significantly higher (P=0.011) than in the late control group. BMI
was not significantly different between the groups, but all groups had
high BMI and the number of obese patients was >50% in all
groups. The mean gestational age in the early groups was significantly
different from the late groups, as expected, and there was no difference
between the mean gestational age of control and PEC cohorts within the
early and late groups.
Systolic arterial pressures were significantly higher in the early and
late PEC groups as compared to the corresponding control groups (Table
1). The diastolic arterial pressure was significantly higher only
between the early PEC and control groups (Table 1). Heart rates were not
significantly different across groups (Table 1).
The estimated MPAP was within the normal reference range (8-20 mmHg) in
the early control group (12.8±6.0 mmHg, mean±S.D. 95% C.I 8.8 – 16.8),
whereas estimated MPAP in the early PEC group was above the normal
reference range (31.4±6.7 mmHg, mean±S.D., 95% C.I. 26.6-36.2) and it
was significantly higher than the early control group (12.8±6.0 mmHg,
mean±S.D., 95% C.I. 9.8-18.0; Fig. 1 A; P<0.0001). Similarly,
estimated MPAP was within the normal reference range in the late control
group (13.9±5.7 mmHg, mean±S.D., 95% C.I. 9.8-18.0). The estimated MPAP
in the late PEC group was slightly above the normal range (22.2±4.9
mmHg, mean±S.D., 95% C.I. 18.5-26.0), and it was significantly
different from the late control group (P=0.024, 95% C.I. 18.5-26.0)
(Fig. 1 A). At a PAAT cut off of 100 ms, there were significantly more
patients with early PEC that had a PAAT < 100 ms compared with
early controls (Table 2). There was no significant difference in the
number of patients with PAAT<100 between late PEC and late
controls (Table 2).
RV MPI was significantly increased in early PEC (0.32±0.11 mmHg,
mean±S.D., 95% C.I. 0.25-0.40) and late PEC (0.36±0.07 mmHg, mean±S.D.,
95% C.I. 0.30-0.41) compared to respective controls(Early control:
0.22±0.06 mmHg, mean±S.D., 95% C.I. 0.18-0.26) and (Late control:
0.25±0.08 mmHg, mean±S.D., 95% C.I. 0.19-0.31) (Figure 1, D). RV FAC,
indexed RV SV, indexed RV CO, MV E/A, MV E/e’, TAPSE and TV S’ were not
significantly different across any of the groups (Table 3). TTAD L was
not significantly different across groups, but TTAD MP, TTAD S and TTAD
MP % were all significantly decreased in early PEC vs early controls
(Table 3) and Figure 2.
The Bland Altman assessment of PAAT between both observers showed a bias
close to 0 (0.455) and the SD of bias was 8.61, revealing that there was
no systematic bias between the two observers (Figure 3). Data shown in
figure1 and supplemental figures 1 and 2 are by the first observer.
Performing the analysis with the data obtained by the second observer
resulted in identical statistical conclusions as performing the analysis
with the data obtained by the first observer (data not shown).
Patients with a history of heart failure or those with EF <
40% were excluded from the study and none of the actual enrolled
subjects had EF <55%. In all of the enrolled patients, LVEF
measured by the area length methodology, LV endocardial fractional
shortening, FAC and lateral mitral annular peak S’ wave velocity were
within normal limits and there were no statistically significant
differences in these parameters of LV function across the groups (data
not shown). Additionally, we assessed whether there are signs of
elevated LA pressure based on recently validated criteria of
E/A>2 or E/e’>14[16]. None of our patients
had an E/A>2 or E/e’>14 that would indicate
elevated left atrial pressure. Additionally, we plotted correlation
between systemic mean arterial pressure (AP) and estimated MPAP (Figure
4). There was no positive correlation between mean AP and estimated
MPAP, indicating that PAP was not simply “tracking” elevation of
systemic pressure.