Because superimposed preeclampsia is not precisely defined in women with chronic hypertension, the reported incidence varies from 13 to 40 percent (American College of Obstetricians and Gynecologists, 2013; Bramham, 2016; Kim, 2016b; Moussa, 2017). August and colleagues (2015) posit that this predilection may stem from similar genetic, biochemical, and metabolic abnormalities. For example, the risk for superimposed preeclampsia is directly related to the severity of baseline hypertension (Ankumah, 2014; Morgan, 2016b). In a Maternal-Fetal Medicine Units (MFMU) Network trial, Caritis and coworkers (1998) identiied superimposed preeclampsia in 25 percent of hypertensive gravidas. he rate was 29 percent in a California database study (Yanit, 2012). And, women whose hypertension becomes severe enough to warrant chronic antihypertensive therapy during pregnancy are at inordinately high risk for superimposed preeclampsia (Morgan, 2016a). And, this risk is even higher if there is baseline proteinuria. Finally, and women at high risk for preeclampsia (Henderson, 2014). The recommendation to initiate 81 mg between 12 and 28 weeks' gestation and continue therapy until delivery was adopted by the American College of Obstetricians and Gynecologists (2016b). In addition to chronic hypertension, indications for aspirin prophylaxis for those at high-risk of preeclampsia include a history ofpreeclampsia, multifetal gestation, diabetes, renal disease, and autoimmune disease.
Antioxidants to prevent preeclampsia have been studied.
with chronic hypertension to treatment with vitamins C and E or with a placebo. A similar number in both groups developed preeclampsia-17 versus 20 percent, respectively.
FIGURE 50-2 Blood pressure trends in treated, chronically hypertensive women with and without superimposed preeclampsia. Mean maternal pressures (MAPs) at entry (p = 0.002) and throughout gestation (p <0.001) are significantly diferent for each group. MAP nadir at 23.3 weeks (95% CI, 22.5-24.1) for superimposed preeclampsia versus 26.4 weeks (95% CI, 22.5-27.6) for those without preeclampsia is significant (3.1 weeks, 95% (I, 2.3-4.3). (Data from Morgan, 2016a.) shown in Figure 50-2, chronically hypertensive women destined to develop severe superimposed preeclampsia have higher initial blood pressures that nadir earlier than those of women who do not develop severe disease.
Thus far, clinical prognostic and predictive tests for superimposed preeclampsia have been disappointing (CondeAgudelo, 2015). Di Lorenzo and colleagues (2012) studied serum markers for Down syndrome to predict preeclampsia and calculated a sensitivity of 60 percent, with a 20-percent false-positive rate. Similar results were found using antiangiogenic factors to discriminate among chronic hypertension, gestational hypertension, and preeclampsia (Costa, 2016; Sibai, 2008). According to Anton and coworkers (2013), microRNA assays may prove valuable as predictors of pregnancy-associated hypertension.
Trials ofvarious medications to prevent preeclampsia in women with chronic hypertension have generally been disappointing and