Abstract TMP53: Preeclampsia Leads to Long Term Cerebral White Matter Damage and Cortical Atrophy: a Magnetic Resonance Imaging Study
Introduction: Women with a history of preeclampsia have a two-fold higher risk of acute ischemic stroke even after controlling for classic cardiovascular risk factors. We determined whether specific patterns in cerebral damage are present after preeclampsia that may explain this risk.
Methods: We performed brain magnetic resonance imaging in women between 5 and 15 years after either a preeclamptic or normotensive pregnancy. Analysis of white matter structure was undertaken using voxel-based segmentation of fluid attenuation inversion recovery sequences to assess white matter lesion volume and diffusion tensor imaging to measure microstructural integrity. Voxel-based analysis of grey matter volumes was performed in T1 weighted sequences with adjustment for skull size. Cardiovascular, obstetric profiles were assessed.
Results: Thirty-four previously preeclamptic women (aged 42.8 ± 5.1 years, mean ± SD) and 49 controls were included. Previously preeclamptic women had reduced cortical grey matter volume (523.2 ± 30.1 vs 544.4 ± 44.7 ml, p<0.05) and, although both groups displayed frontal white matter damage, changes were more extensive in previously preeclamptic women. They displayed increased temporal lobe white matter disease (lesion volume: 23.2 ± 24.9 vs 10.9 ± 15.0 ml, p<0.05) and altered microstructural integrity (radial diffusivity 538 ± 19 vs. 526 ± 18*10-6 mm2/sec, p<0.01), which also extended to occipital and parietal lobes. The degree of temporal lobe white matter change in previously preeclamptic women was independent of their current cardiovascular risk profile (p<0.05) and increased with time from index pregnancy (Figure).
Conclusions: A history of preeclampsia is associated with temporal lobe white matter damage and cortical atrophy in young women, which is out of proportion to their classic cardiovascular risk profile and increases with time from pregnancy, consistent with ongoing susceptibility and cumulative brain damage.
Author Disclosures: T. Siepmann: None. H. Boardman: None. A. Bilderbeck: None. L. Griffanti: None. Y. Kenworthy: None. C. Zwager: None. D. McKean: None. J. Francis: None. S. Neubauer: None. G.Z. Yu: None. A. Lewandowski: None. Y.B. Sverrisdottir: None. P. Leeson: None.
- © 2017 by American Heart Association, Inc.