Background Women with a history of preeclampsia (hxPE) exhibit sustained arterial stiffness and elevated blood pressure (BP) postpartum. Aortic stiffness and 24-hour BP variability (BPV) are associated with age-related cognitive decline. Although hxPE is related to altered cognitive function, the association between aortic stiffness and BPV with cognitive performance in young women with hxPE has not been investigated. The objectives of this study were to 1) test whether cognitive performance is lower in young women with hxPE and 2) determine whether aortic stiffness and BPV are associated with cognitive performance independent of 24-hour average BP. Methods Women with hxPE (N=23) and healthy pregnancy controls (N=38) were enrolled 1-3 years postpartum. Cognitive performance was assessed in domains of memory, processing speed and executive function. 24-hour ambulatory BP monitoring and carotid-femoral pulse wave velocity (cfPWV) were used to measure BPV and aortic stiffness, respectively. Results Women with hxPE had slower processing speed (-0.56±0.17 versus 0.34±0.11 Z-score, P<0.001) and lower executive function (-0.43±0.14 versus 0.31±0.10 Z-score, P=0.004) compared with controls independent of education, whereas memory did not differ. BPV and cfPWV (adjusted for BP) did not differ between women with hxPE and controls. Greater diastolic BPV was associated with lower executive function independent of 24-hour average BP and education in women with hxPE (r = -0.48, P=0.03) but not controls (r = 0.15, P=0.38). Conclusions Select cognitive functions are reduced postpartum in young women with a recent hxPE and linked with elevated 24-hour diastolic BPV.

Women with preeclampsia, a hypertensive disorder of pregnancy, exhibit greater beat-to-beat blood pressure variability (BPV) in the third trimester after clinical onset of the disorder. However, it remains unknown whether elevated BPV precedes the development of preeclampsia. A prospective study cohort of 139 women (age 30.2±4.0 years) were enrolled in early pregnancy (<14 weeks gestation). BPV was quantified by time domain analyses of 10-minute continuous beat-to-beat blood pressure recordings via finger photoplethysmography in the first, second, and third trimesters. Aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal baroreflex sensitivity were also measured each trimester. Eighteen women (13%) developed preeclampsia. Systolic BPV was higher in all trimesters among women who developed versus did not develop preeclampsia (first: 4.8±1.3 versus 3.7±1.2, P =0.001; second: 5.1±1.8 versus 3.8±1.1, P =0.02; third: 5.2±0.8 versus 4.0±1.1 mm Hg, P =0.002). Elevated first trimester systolic BPV was associated with preeclampsia (odds ratio, 1.94 [95% CI, 1.27–2.99]), even after adjusting for risk factors (age, body mass index, systolic blood pressure, history of preeclampsia, and diabetes mellitus) and was a significant predictor of preeclampsia (area under the receiver operator characteristic curve=0.75±0.07; P =0.002). Carotid-femoral pulse wave velocity was elevated in the first trimester among women who developed preeclampsia (5.9±0.8 versus 5.2±0.8 m/s; P =0.002) and was associated with BPV after adjustment for mean blood pressure ( r =0.26; P =0.005). First trimester baroreflex sensitivity did not differ between groups ( P =0.23) and was not related to BPV ( P =0.36). Elevated systolic BPV is independently associated with the development of preeclampsia as early as the first trimester, possibly mediated in part by higher aortic stiffness.

Preeclampsia is a hypertensive disorder of pregnancy effecting ∼5–8% of pregnancies in the United States, and ∼8 million pregnancies worldwide. Preeclampsia is clinically diagnosed after the 20th week of gestation and is characterized by new onset hypertension accompanied by proteinuria and/or thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or cerebral or visual symptoms. This broad definition emphasizes the heterogeneity of the clinical presentation of preeclampsia, but also underscores the role of the microvascular beds, specifically the renal, cerebral, and hepatic circulations, in the pathophysiology of the disease. While the diagnostic criteria for preeclampsia relies on the development of de novo hypertension and accompanying clinical symptoms after 20-week gestation, it is likely that subclinical dysfunction of the maternal microvascular beds occurs in parallel and may even precede the development of overt cardiovascular symptoms in these women. However, little is known about the physiology of the non-reproductive maternal microvascular beds during preeclampsia, and the mechanism(s) mediating microvascular dysfunction during preeclamptic pregnancy are largely unexplored in humans despite their integral role in the pathophysiology of the disease. Therefore, the purpose of this review is to provide a summary of the existing literature on maternal microvascular dysfunction during preeclamptic pregnancy by reviewing the functional evidence in humans, highlighting potential mechanisms, and providing recommendations for future work in this area.

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Objective: Central (abdominal) obesity is associated with elevated adrenergic activity and arterial blood pressure (BP). Therefore, we tested the hypothesis that transduction of spontaneous muscle sympathetic nerve activity (MSNA) to BP, that is, sympathetic transduction, is augmented in abdominal obesity (increased waist circumference) and positively related to prevailing BP.Methods: Young/middle-aged obese (32 AE 7 years; BMI: 36 AE 5 kg/m 2 , n ¼ 14) and nonobese (29 AE 10 years; BMI: 23 AE 4 kg/m 2 , n ¼ 14) without hypertension (24-h ambulatory average BP < 130/80 mmHg) were included. MSNA (microneurography) and beat-to-beat BP (finger cuff) were measured continuously and the increase in mean arterial pressure (MAP) during 15 cardiac cycles following MSNA bursts of different patterns (single, multiples) and amplitude (quartiles) was signal-averaged over a 10 min baseline period.Results: MSNA burst frequency was not significantly higher in obese vs. nonobese (21 AE 3 vs. 17 AE 3 bursts/min, P ¼ 0.34). However, resting supine BP was significantly higher in obese compared with nonobese (systolic: 127 AE 3 vs. 114 AE 3; diastolic: 76 AE 2 vs. 64 AE 1 mmHg, both P < 0.01). Importantly, obese showed greater increases in MAP following multiple MSNA bursts (P ¼ 0.02) and MSNA bursts of higher amplitude (P ¼ 0.02), but not single MSNA bursts (P ¼ 0.24), compared with nonobese when adjusting for MSNA burst frequency. The increase in MAP following higher amplitude bursts among all participants was associated with higher resting supine systolic (R ¼ 0.48; P ¼ 0.01) and diastolic (R ¼ 0.48; P ¼ 0.01) BP when controlling for MSNA burst frequency, but not when also controlling for waist circumference (P > 0.05). In contrast, sympathetic transduction was not correlated with 24-h ambulatory average BP. Conclusion:Sympathetic transduction to BP is augmented in abdominal obesity and positively related to higher resting supine BP but not 24-h ambulatory average BP.