Individuals who are born pre term have greater ventricular mass later in life (Lewandowski, 20l3). And, women who have preeclampsia and who develop chronic hypertension later in life have an increased ventricular mass index before they become hypertensive (Ghossein-Doha, 2013). Finally, in at least some of these women, hypertensive cardiovascular pathologies appear to have begun near the time of their own births. A similar phenomenon is associated with preterm birth and with fetal-growth disorders.
Preeclampsia is also a marker for subsequent renal disease. lmost 15 percent of previously preeclamptic women have renal dysfunction (Lopes van Balen, 2017). In a 40-year study of Norwegian birth and end-stage renal disease linked registries, although the absolute risk of renal failure was small, preeclampsia was associated with a fourfold greater risk (Vikse, 2008). Women with recurrent preeclampsia had an even higher risk. These data need to be considered in light of the indings that 15 to 20 percent of women with preeclampsia who undergo renal biopsy have evidence of chronic renal disease (Chesley, 1978). In another long-term study, Spaan and coworkers (2009) compared formerly preeclamptic women with a cohort of women who were normotensive at delivery. At 20 years following delivery, preeclamptic women were signiicantly more likely to be chronically hypertensive-55 versus 7 percent-compared with control women. They also had higher peripheral vascular and renovascular resistance and decreased renal blood low. These data do not permit conclusions as to cause versus efect.
Until recently, eclamptic seizures were believed to have no signiicant long-term sequelae. However, this may not be the case (heilen, 2016). Recall that almost all eclamptic women have multifocal areas of perivascular edema, and approximately a fourth also have areas of cerebral infarction (Zeeman, 2004a).
In several long-term follow-up studies in women with severe preeclampsia and eclampsia, brain white-matter lesions that followed eclamptic convulsions persist (Aukes, 2007, 2009, 2012). Speciically, when studied with MR imaging at a mean of 7 years, 40 percent of formerly eclamptic women had more numerous and larger aggregate white matter lesions compared with 17 percent of normotensive control women. These investigators later also observed these white-matter lesions in preeclamptic women without convulsions (Aukes, 2012). And, Siepmann and associates (2017) documented temporal lobe white matter changes and reduced cortical volume in previously preeclamptic women. In studies designed to assess clinical relevance, formerly eclamptic women had subjectively impaired cognitive functioning (Postma, 2014). Wiegman and associates (2012) reported that formerly eclamptic women at approximately 10 years had lower vision-related quality of life compared with control subjects. This likely coincides with an elevated risk for retinopathy described by Auger and colleagues (2017). Because no baseline studies were done before these women sufered from preeclampsia or eclampsia, the investigators appropriately concluded that a cause versus an efect of these white-matter lesions remains unknown.
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