Differences in cardiovascular function comparing prior preeclamptics with nulliparous controls

- There are significant differences in cardiovascular dynamics in women with a history of preterm preeclampsia compared to nulliparous women not explained by prior pregnancy.
- Previous preterm preeclamptics exhibit an underlying physiologic relationship between blood pressure and arterial stiffness not observed in women with prior normal pregnancy.
- Vascular compliance appears to be reduced in women with prior preterm preeclampsia.

ObjectiveThe objective of the current study was to evaluate cardiovascular function; including blood pressure, cardiac output, pulse wave velocity and vascular compliance in nonpregnant nulliparous women compared to women with a history of preterm preeclampsia.Study designThis was a case control study. Blood pressure was measured using the Finapres Pro. Baseline cardiac output was determined by echocardiography. Pulse wave velocity was estimated using simultaneous electrocardiographic tracings and ultrasound determined arterial flow waveforms and calculated as estimated distance divided by the time interval between EKG r-wave peak and ultrasound derived peak popliteal artery flow. During volume challenge, 500 mL of lactated Ringers solution was infused through an indwelling antecubital catheter over 10 min. Cardiac output and blood pressure during and 15 min after the infusion were estimated using the Finapres Pro.Main outcome measuresIndices of arterial stiffness and vascular compliance.ResultsPrevious preeclamptics exhibited a significant increase in pulse pressure and cardiac output in response to volume challenge when compared with nulliparous controls. Prior preeclamptics had a strong positive correlation between blood pressure indices (r = 0.50-0.68, p ⩽ 0.01) and pulse pressure (r = 0.58, P = 0.008) with pulse wave velocity that was not evident in control women.ConclusionsIn women with prior preterm preeclampsia a relationship between blood pressure, intravascular volume and arterial stiffness, is evident in the nonpregnant state and in the absence of hypertension or overt cardiovascular disease. This supports an overarching hypothesis that nonpregnant physiology is an important contributor to pregnancy adaptations.