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Blood Pressure Variability during Early‐Mid Pregnancy in Women Who Develop Preeclampsia: Association with Aortic Stiffness but not Baroreflex Sensitivity
Author(s) -
Nuckols Virginia,
Holwerda Seth,
DuBose Lyndsey,
O'Deen Allison,
Stroud Amy,
Luehrs Rachel,
Brandt Debra,
Santillan Mark,
Grobe Justin L,
Santillan Donna,
Pierce Gary
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.856.2
Subject(s) - medicine , preeclampsia , blood pressure , cardiology , baroreflex , arterial stiffness , pulse wave velocity , pregnancy , systole , mean blood pressure , hemodynamics , diastole , heart rate , genetics , biology
Background Preeclampsia (PE) is associated with a four‐fold increased risk of developing hypertension later in life. Hemodynamic adaptations to normal pregnancy involve a reduction large artery (e.g., aortic) stiffness and changes in autonomic control such as reduced baroreflex sensitivity (BRS), both of which influence blood pressure variability (BPV). BPV is higher during late pregnancy in women who develop PE; however, it remains unclear the extent to which vascular stiffness and BRS contribute to BPV during pregnancy in women who develop PE. We hypothesized that beat‐to‐beat BPV would be elevated in early‐mid gestation in women who develop PE prior to the onset of clinical PE and that greater BPV would be related to lower BRS and higher aortic stiffness. Methods Nine women who developed PE in late 3 rd trimester and fifty‐four healthy pregnancy controls (31 ± 1.4 vs 30 ± 0.4 yrs, p=0.18) were assessed in the 1 st (12 ± 0.1 wks), 2 nd (22 ± 0.3 wks) and 3 rd trimester (32 ± 0.3 wks). BPV and BRS were measured continuously for 10 minutes by finger plethysmography and electrocardiography. BPV was calculated as the standard deviation of beat‐by‐beat mean arterial pressure. BRS was calculated as the change in R‐R interval per unit change in blood pressure (ms/mmHg) via the sequence technique. Large artery stiffness was measured by applanation tonometry expressed as carotid‐femoral pulse wave velocity (CFPWV). Results Women who developed PE had higher BPV in the 1 st (4.43 ± 0.6 vs 3.07 ± 0.1 mmHg, p=0.02) and 2 nd (4.05 ± 0.4 vs 3.05 ± 0.1 mmHg, p=0.01) trimester after adjusting for mean arterial pressure (MAP), but not in the 3 rd trimester (4.70 ± 0.7 vs 3.37 ± 0.1 mmHg, p=0.95). In the entire cohort (n=63), there were reductions in BRS (ms/mmHg) between the 1 st (20.4 ± 1.1), 2 nd (14.5 ± 1.1) and 3 rd (11.9 ± 0.9) trimester (p<0.001), but BRS did not differ between PE or controls. Therefore, BPV was higher in PE compared with normal pregnancy and did not change while cardiovagal BRS was progressively reduced in both PE and normal pregnancy. Importantly, women who developed PE had higher CFPWV in the 1 st (5.9 ± 0.3 vs 5.2 ± 0.1 m/s, p=0.02) and 3 rd (6.1 ± 0.4 vs 5.0 ± 0.1 m/s, p<0.01) trimesters. After adjusting for MAP, CFPWV was correlated with BPV in women with PE (r=0.77, p<0.05) but not in controls (r=0.13, p=0.37) in the 1 st trimester. Conclusions Beat‐to‐beat BPV and aortic stiffness were elevated during early‐mid pregnancy in PE while cardiovagal BRS was reduced similarly in women with PE and normal pregnancy. Therefore, these preliminary findings suggest that higher aortic stiffness may be an important contributor to dysregulation of blood pressure in women that develop PE. Support or Funding Information AHA 15SFRN2373000 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .