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• W4200430911 abstract "Through the ASPRE (Combined Multimarker Screening and Randomized Patient Treatment with Aspirin for Evidence-Based Pre-eclampsia Prevention) trial, we have demonstrated that aspirin prophylaxis given to high-risk women, identified by first-trimester combined screening based on maternal factors, mean arterial pressure (MAP), uterine artery Doppler, serum pregnancy-associated plasma protein-A and serum placental growth factor (PlGF), achieved a 62% reduction in the incidence of preterm pre-eclampsia1. In other words, 38% of high-risk women develop preterm pre-eclampsia despite aspirin treatment. As highlighted by Giorgione et al., a recent implementation study has demonstrated that, through an interrupted time-series analysis, the ASPRE screening and prophylaxis protocol achieves an estimated 80% effect size reduction in preterm pre-eclampsia2. Essentially, the authors reported similar results to those of the ASPRE trial, which showed that aspirin cannot achieve 100% prevention of preterm pre-eclampsia. We should not be complacent about the success of the ASPRE trial as it represents merely the beginning of a new paradigm, in which early effective prediction and prevention of pregnancy complications can be achieved. In response to the statistical issues raised by Giorgione et al., the findings of the variance inflation factor (VIF) analysis of MAP multiples of the median (MoM) and chronic hypertension were what we expected, showing that MAP MoM was collinear with chronic hypertension. A VIF of 40.96 demonstrated this multicollinearity. Therefore, it was necessary to remove MAP MoM from the model, leaving only chronic hypertension3. Of note, saying that a history of chronic hypertension is defined by high MAP would be to assume that participants with chronic hypertension had higher MAP MoM at the time of screening, which is, in fact, not necessarily true. There are essentially two presentations of chronic hypertension. First, women who are diagnosed before pregnancy who may be on antihypertensive agents for hypertension management and may therefore be normotensive at the time of screening. Second, women who present with hypertension at the time of screening and are subsequently diagnosed with chronic hypertension. Amongst the high-risk women in the ASPRE trial, there was no statistical difference in MAP MoM between those with chronic hypertension and those without (1.079 vs 1.081; P = 0.920). In our study4, table 2 demonstrates clearly that PlGF MoM, as a continuous variable, is predictive of preterm pre-eclampsia amongst high-risk women treated with aspirin. The subgroup analyses (tables 3 and 4) explored the key contributors to preterm pre-eclampsia development in the three risk categories. PlGF MoM had an inverse relationship with estimated risk for preterm pre-eclampsia, i.e. the lower the PlGF MoM, the higher the estimated risk. The finding that PlGF MoM was not predictive of preterm pre-eclampsia in women with estimated risks of 1 in 11 to 1 in 50 and 1 in 51 to 1 in 100 is not surprising, firstly, because of the lower rates of preterm pre-eclampsia in these risk groups (3.13% and 0.94%, respectively) compared to the group with an estimated risk of 1 in 2 to 1 in 10 (9.78%) and, secondly, because the separation of the PlGF MoM distributions between unaffected and affected cases in these risk groups was smaller compared to the very high-risk group. The PlGF cut-off of 0.712 MoM was chosen as the optimal threshold using non-parametric receiver-operating-characteristics-curve analysis. The actual rates of preterm pre-eclampsia were 2.4% and 0.8% in women with PlGF < 0.712 MoM and ≥ 0.712 MoM, respectively, corresponding to the reported adjusted odds ratio in table 5. There were 48 cases of preterm pre-eclampsia and, therefore, having four variables (trial drug, history of chronic hypertension, PlGF and estimated risk) in the prediction model was appropriate according to the rule of 10. Our intentions in this secondary analysis of the ASPRE data were two-fold4. First, to identify those who are at risk of subsequent development of preterm pre-eclampsia following aspirin treatment. Second, to drive future research to identify novel biomarkers for improved prediction and alternative therapeutic interventions. We have shown that women with very high estimated risks of 1 in 2 to 1 in 10 and 1 in 11 to 1 in 50 are more likely to develop preterm pre-eclampsia despite aspirin prophylaxis, in comparison to those with an estimated risk of 1 in 51 to 1 in 100. These findings are not surprising and are analogous to those observed with the use of vaginal progesterone in the prevention of spontaneous preterm birth, namely that the intervention is not as effective in women with cervical length below 10 mm as it is in those with a length of 10–20 mm. Previously, Wright and Nicolaides5 reported exploratory data from the ASPRE trial in support of the hypothesis that aspirin prevents pre-eclampsia by delaying delivery. By delaying the onset of pre-eclampsia, more cases of term pre-eclampsia arise from pregnancies that were destined to develop preterm pre-eclampsia, resulting in a significant reduction in the rate of preterm pre-eclampsia but not the rate of term pre-eclampsia. Very recently, a study utilizing untargeted metabolomic analysis of plasma samples of aspirin/placebo-treated ASPRE trial participants has demonstrated that aspirin decreases significantly the metabolic clock-estimated gestational age. In addition, aspirin treatment partially reversed a wide range of metabolic changes over gestation, lending further support to our hypothesis that the benefit of aspirin treatment in preventing pre-eclampsia is mediated through decelerating the metabolic clock of gestation6. Based on these findings, we believe that women with a very high-risk result for preterm pre-eclampsia can still benefit from aspirin prophylaxis and that, despite a delay in the disease onset, delivery still occurs before 37 weeks' gestation. We should recognize that the beneficial effect of aspirin cannot be assessed simply according to the relative reduction in the rate of pre-eclampsia with delivery at a certain gestational-age cut-off. In our clinical practice, we are moving away from stating simply that aspirin is effective in preventing preterm pre-eclampsia. We explain that the benefit of aspirin is mediated via a delay in the onset of the disorder and, therefore, of delivery with pre-eclampsia. It is crucial that every effort is made to identify patients who may still develop pre-eclampsia despite aspirin prophylaxis because they should be provided with appropriate advice to be vigilant of pre-eclampsia symptoms and seek medical attention, when necessary." @default.
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• W4200430911 date "2021-10-01" @default.
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• W4200430911 doi "https://doi.org/10.1002/uog.24761" @default.
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