Arterial stiffness but not physical activity levels and vascular endothelial function are altered in early/mid pregnancy in women who develop preeclampsia

Abstract

Preeclampsia is a pregnancy disorder that effects ~5–8% of all pregnancies and is characterized by de novo hypertension, proteinuria and multiple organ dysfunction in late gestation. Higher levels of leisure time physical activity (LTPA) are associated with lower risk of preterm delivery and preeclampsia in pregnancy. Women who develop preeclampsia demonstrate increased central artery stiffness and vascular endothelial dysfunction in early/mid gestation before clinical signs/symptoms of preeclampsia manifest. Therefore, we hypothesized that 1) higher total LTPA would be associated with lower arterial stiffness and higher vascular endothelial function during each trimester in pregnant women, and 2) compared with normal pregnancy, women who develop preeclampsia would demonstrate lower LTPA, higher arterial stiffness and lower endothelial function in early/mid gestation before signs of preeclampsia manifest. We enrolled 130 pregnant women in the first trimester (age 29.8 ± 0.4 yrs; BMI 28 ± 0.7 kg/m2) and studied them prospectively in the 1st (n=130; 11.8 ± 0.1 weeks gestation), 2nd (n=97; 22 ± 0.2 weeks) and 3rd (n=59; 34.2 ± 0.3 weeks) trimesters and obtained pregnancy outcomes (i.e., developed preeclampsia vs. normal pregnancy). Total LTPA (Pregnancy Physical Activity Questionnaire) in metabolic equivalents (MET‐hrs/week), carotid artery β‐stiffness (carotid ultrasound and tonometry), aortic stiffness (carotid‐femoral pulse wave velocity, CFPWV) and endothelial function (brachial artery flow‐mediated dilation, FMD) were assessed each trimester. In the entire cohort, there was no association between total LTPA and carotid β‐stiffness, CFPWV, FMD or BP in 1st (all P>0.05), 2nd (all P>0.05) or 3rd (all P>0.05) trimesters, respectively. Out of the 104 women who delivered, 9 (8.7%) developed preeclampsia. Because 6 women in the preeclampsia group delivered prematurely, only 1st and 2nd trimester comparisons were made between the preeclampsia and normal pregnancy groups. There was no difference in LTPA between preeclampsia and normal pregnancy in the 1st (204 ± 31 vs. 182 ± 7 MET‐hrs/wk, P=0.41) and 2nd (145 ± 30 vs. 175 ± 8 MET‐hrs/wk, P=0.33) trimesters. In contrast, CFPWV and systolic BP were elevated in the 1st (5.9 ± 0.4 vs. 5.2 ± 0.1 m/sec, P=0.03; 121 ± 5 vs. 109 ± 0.9 mmHg P<0.01) and 2nd (5.8 ± 0.6 vs. 4.9 ± 0.1m/sec, P<0.01; 126 ± 5 vs. 106 ± 0.9 mmHg, P<0.01) trimesters in preeclampsia and normal pregnancy, but carotid β‐stiffness was only elevated in the 1st trimester (7.42 ± 1.4 vs. 5.96 ± 0.17 U, P=0.05). Brachial artery FMD was not different between groups in 1st or 2nd trimester (both P>0.05). These preliminary data suggest that LTPA is not associated with arterial stiffness or endothelial function throughout pregnancy and that LTPA is not lower in early/mid gestation in women who develop preeclampsia. Central artery stiffness and BP are elevated early in pregnancy in women who develop preeclampsia months before clinical signs/symptoms manifest.Support or Funding InformationAmerican Heart Association (15SFRN23730000; 17POST334410101), American Physiology Society STRIDE undergraduate summer research fellowship; National Institutes of Health (T32HL007121).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.