Cardiovascular effects of severe late-onset preeclampsia are reversed within six months postpartum

Preeclampsia (PE) is a common pregnancy-related disorder associated with cardiovascular long-term disease. Eighty percent are late-onset PE, occurring after 34 gestational weeks, and can present with severe symptoms. Magnitude and reversibility rate of maternal cardiovascular changes after severe late-onset PE have not been characterized. This study therefore evaluated longitudinal dynamics of maternal cardiovascular changes after severe late-onset PE.

Six previously normotensive women with severe late-onset PE and eight pregnant controls were included. Severe PE was defined as systolic blood pressure (SBP) ≥ 160 mmHg or diastolic blood pressure (DBP) ≥ 110 mmHg and proteinuria with/without evidence of end-organ dysfunction, or SBP ≥ 140 mmHg or DBP ≥ 90 mmHg with/without proteinuria and with evidence of end-organ dysfunction. Cardiovascular function was assessed by magnetic resonance imaging at 1-3 days, one week and six months postpartum.

Left ventricular mass at 1-3 days postpartum was higher after severe late-onset PE (57 g/m²) compared to after normal pregnancy (48 g/m²; p = 0.01). Pulse wave velocity (PWV) decreased between 1 and 3 days and six months postpartum after PE (6.1 to 5.0 m/s; p = 0.028). There was no difference in PWV 1-3 days postpartum after severe PE compared after normal pregnancy (6.1 versus 5.6 m/s; p = 0.175). Blood pressure normalized within six months in all but one patient.

Cardiac effects after severe late-onset PE were small and transient. This indicates that left ventricular hypertrophy after severe late-onset PE may be a secondary physiologic response to increased peripheral resistance in PE. Vascular mechanisms rather than persistent cardiac hypertrophy postpartum may be the culprit for increased long-term cardiovascular risk after PE.