Increased carotid artery stiffness after preeclampsia in a cross-sectional study of postpartum women.

Preeclampsia (PE) is a hypertensive obstetrical complication associated with increased cardiovascular disease risk. Carotid artery functional assessments allow for identification of subclinical vascular dysfunction. This cross-sectional study measured carotid artery functional indices in healthy women with a recent pregnancy complicated by PE, versus women with a prior uncomplicated pregnancy. Women with a history of PE (N = 30) or an uncomplicated pregnancy (N = 30), were recruited between 6 months and 5 years postpartum. Left and right carotid artery ultrasound measured carotid intima media thickness, plaque burden, peak systolic velocity, end diastolic flow velocity and carotid far-wall circumferential strain (FWCS). Carotid FWCS is inversely related to vessel stiffness, where a decrease in FWCS indicates increased vessel stiffness. Right-side FWCS did not differ between women with a history of PE versus normotensive pregnancy. Left carotid artery FWCS was lower in formerly preeclamptic women after adjustment for diameter, pulse pressure, and heart rate compared to women following an uncomplicated pregnancy (3.35 ± 1.08 × 10-3 vs. 4.46 ± 1.40 × 10-3 ; p = 0.003). Those with prior severe PE had the greatest decrease in FWCS adjusted to diameter, pulse pressure, and heart rate compared to healthy controls (p = 0.02). Adjusted FWCS and total serum cholesterol were independent indicators of PE history when present in a logistic regression model with confounding variables including age, body mass index, and resting blood pressure. Further investigation is needed to elucidate if FWCS can be used as a risk stratification tool for future cardiovascular disease following a pregnancy complicated by PE. A history of PE is associated with decreased left FWCS (increased left carotid artery stiffness).

Maternal Cardiovascular Function Following a Pregnancy Complicated by Preeclampsia.

Preeclampsia is a hypertensive pregnancy complication with an unknown etiology and high maternal burden worldwide. Burgeoning research has linked preeclampsia to adverse maternal health outcomes remote from pregnancy; however, the intermediary mechanisms responsible for this association have not been sufficiently established. In the present narrative review, we summarize leading evidence of structural and functional cardiovascular changes associated with prior preeclampsia, and how these changes may be linked to future maternal disease. KEY POINTS: · Prior preeclampsia is associated with subclinical structural and functional vascular changes remote from pregnancy.. · Maternal cardiac adaptations to preeclampsia may have long-term implications on cardiovascular health.. · Clinicians have an opportunity to minimize maternal disease risk following preeclampsia..

Postpartum microvascular functional alterations following severe preeclampsia.

Preeclampsia is associated with adverse maternal health outcomes later in life. Vascular endothelial dysfunction has been previously described following preeclampsia. We hypothesized that microvascular endothelial dysfunction associated with preeclampsia persists postpartum and may identify those at greatest risk of future cardiovascular disease. The objective of this study was to examine postpartum microvascular endothelial function in women after a pregnancy complicated by preeclampsia. Women with previous preeclampsia (n = 30) and normotensive controls (n = 30) between 6 mo and 5 yr postpartum were recruited. Severity of preeclampsia [severe (n = 16) and mild (n = 14)] was determined by standardized chart review. Microvascular reactivity in the forearm was measured with laser speckle contrast imaging, coupled with iontophoresis; endothelium-dependent and endothelium-independent vasodilation was induced with 1% acetylcholine and sodium nitroprusside solutions, respectively. A postocclusive reactive hyperemia test assessed vasodilatory response following three minutes of suprasystolic (200 mmHg) occlusion with a mechanized cuff. Women with prior severe preeclampsia exhibited significantly higher vasodilation to acetylcholine and sodium nitroprusside compared to controls (P < 0.01; P = 0.03) and prior mild preeclampsia (P = 0.03; P < 0.01). Neither the degree of postocclusive reactive hyperemia (P = 0.98), nor time to return halfway to baseline [OR = 1.026 (0.612, 1.72); P = 0.92], differed between preeclampsia and controls. In conclusion, severe preeclampsia is associated with heightened postpartum microvascular endothelium-dependent and endothelium-independent vasoreactivity. These changes, or a common antecedent, may be linked to postpartum alterations in vascular function that predispose women to disease after preeclampsia. Further investigation should identify the contributing mechanism and the degree to which it could be amenable to medical intervention.NEW & NOTEWORTHY We examine maternal microvascular function after preeclampsia, identifying heightened endothelium-dependent and endothelium-independent microvascular reactivity following severe disease. Our study represents a noteworthy addition to the existing literature with the use of a novel imaging modality, vascular perturbation, postpartum time point, and patient population with differentiation of preeclampsia into severe and nonsevere subtypes. These results represent a novel addition to the growing clinical and academic understanding of maternal health outcomes following preeclampsia.