Key result
Severe late-onset preeclampsia resulted in no significant difference in pulse wave velocity 1-3 days postpartum compared to normal pregnancy (6.1 vs 5.6 m/s; p=0.175).
Why the study?
The magnitude and reversibility rate of maternal cardiovascular changes after severe late-onset preeclampsia have not been characterized.
Does severe late-onset preeclampsia cause persistent maternal cardiovascular changes at six months postpartum compared to normal pregnancy?
Observational (n=14)
Does severe late-onset preeclampsia cause persistent maternal cardiovascular changes at six months postpartum compared to normal pregnancy?
Cardiac effects after severe late-onset preeclampsia are small and transient, normalizing within six months postpartum, suggesting that vascular mechanisms rather than persistent cardiac hypertrophy drive long-term cardiovascular risk.
Transient PWV changes after severe late-onset preeclampsia normalize by six months; leaves open drivers of long-term maternal cardiovascular risk.
OBJECTIVES: 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. STUDY DESIGN: 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. RESULTS: ; 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. CONCLUSIONS: 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.
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Kalapotharakos et al. (2020) conducted an observational in Severe late-onset preeclampsia (n=14). Severe late-onset preeclampsia vs. Normal pregnancy was evaluated on Pulse wave velocity (PWV) 1-3 days postpartum (p=0.175). Severe late-onset preeclampsia resulted in no significant difference in pulse wave velocity 1-3 days postpartum compared to normal pregnancy (6.1 vs 5.6 m/s; p=0.175).
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