Pregnancy induces rapid, progressive, and substantial changes to the cardiovascular system. The low recurrence risk of preeclampsia, despite familial predisposition, suggests an adaptation associated with pregnancy that attenuates the risk for subsequent preeclampsia. We aimed to evaluate the persistent effect of pregnancy on maternal cardiovascular physiology.

Forty-five healthy nulliparous women underwent baseline cardiovascular assessment before conception and repeated an average of 30 months later. After baseline evaluation, 17 women conceived singleton pregnancies and all delivered at term. The remaining 28 women comprised the nonpregnant control group. We measured mean arterial blood pressure, cardiac output, plasma volume, pulse wave velocity, uterine blood flow, and flow-mediated vasodilation at each visit.

There was a significant decrease in mean arterial pressure from the prepregnancy visit to postpartum in women with an interval pregnancy (prepregnancy, 85.3 ± 1.8; postpartum, 80.5 ± 1.8 mm Hg), with no change in nonpregnant control subjects (visit 1, 80.3 ± 1.4; visit 2, 82.8 ± 1.4 mm Hg) (P = .002). Pulse wave velocity was significantly decreased in women with an interval pregnancy (prepregnancy, 2.73 ± 0.05; postpartum, 2.49 ± 0.05 m/s), as compared with those without an interval pregnancy (visit 1, 2.56 ± 0.04; visit 2, 2.50 ± 0.04 m/s) (P = .005). We did not observe a residual effect of pregnancy on cardiac output, plasma volume, uterine blood flow, or flow-mediated vasodilation.

Our observations of decreased mean arterial pressure and reduced arterial stiffness following pregnancy suggest a significant favorable effect of pregnancy on maternal cardiovascular remodeling. These findings may represent a mechanism by which preeclampsia risk is reduced in subsequent pregnancies.