Arterial health abnormalities in women with pre-eclampsia: contributing role of central obesity

Abstract

Abstract Introduction Women who suffer from pre-eclampsia (PE) are at higher risk of developing cardiovascular disease (CVD) later in life. This risk can be explained in part by the observation of worse arterial health in these women, with PE either acting as a cause or harbinger of a worse baseline risk profile. Central obesity (CO) is an established risk factor for PE, while it also adversely affects cardiovascular risk. However, whether CO contributes to further worsening of arterial hemodynamics in pre-eclamptic women remains unclear. Purpose To evaluate the effect of CO combined with previous PE on women's arterial hemodynamics. Methods We studied 40 women with history of PE <6 years and 40 age-matched women with previous normotensive pregnancy (controls) in the same timeframe. We estimated aortic stiffness, central blood pressure, and measures of steady and pulsatile arterial load with validated techniques combining applanation tonometry and transthoracic echocardiography. CO was defined as a waist-to-hip ratio (WHR) ≥0.85 according to WHO criteria for women. Differences in arterial hemodynamics across the 3 groups [PE with CO (PE-CO), PE without CO (PE-noCO), controls] were assessed with One-Way ANOVA, and in multivariable linear regression models adjusted for age, hypertension, diabetes, serum creatinine, and parity. Results Twenty-six (65%) of the PE women had CO, compared to 18 (45%) of controls (p=0.07). Patient characteristics are described in the Table. In unadjusted analyses, PE-CO women had higher central systolic blood pressure as compared to PE-noCO and controls respectively (117±21 vs 100±12 and 95±9 mmHg, p<0.01), as well as higher carotid-femoral pulse wave velocity (6.58±0.97 vs 5.95±1.01 and 5.68±0.75 m/s, p<0.01) and forward pressure wave amplitude (42.32±11.16 vs 33.31±6.85 and 37.12±8.70 mmHg, p=0.01), with lower proximal aortic compliance (8.56±3.19 vs 11.47±0.95 and 11.06±3.59x10–6 cm4/dyne, p=0.01) and total arterial compliance (1.38±0.42 vs 1.74±0.53 and 1.71±0.45 mL/mmHg, p=0.01). (Figure) After adjustment for potential confounders in multivariable linear regression, PE-CO women had higher central systolic blood pressure (mean difference [MD] = 10±2.5 mmHg, p<0.01), carotid-femoral pulse wave velocity (MD = 0.42±0.15 m/s, p<0.01) and lower proximal aortic compliance (MD = −1.13±0.63x10–6 cm4/dyne, p=0.04) as compared to controls, while hemodynamics of PE-noCO did not significantly differ from controls. Conclusion We demonstrate for the first time the contribution of CO in adversely affecting arterial health and central hemodynamics in women with PE. Conversely, women with prior PE who did not have CO had similar arterial hemodynamics as compared to women with normotensive pregnancies. Understanding that worse arterial stiffness and hemodynamics are linked to future CVD, our results suggest that PE-CO may represent a higher risk subgroup who may be candidates for early, targeted efforts at primary prevention of CVD. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Heart Team Grant from the University of Ottawa Heart Institute Foundation