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 Six patients were excluded due to: Delivery at another institution (2), withdrawn consent (2), technical difficulties with echo (1) non-reassuring fetal heart tones (1), leaving 40 patients for final analysis.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.