Department of Obstetrics and Gynecology, Oslo University Hospital, Ulleval, Oslo, Norway.
Hypertension. 2011 Jul;58(1):63-9. doi: 10.1161/HYPERTENSIONAHA.111.172387. Epub 2011 May 23.
Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P<0.001; children: P<0.05). Postpartum maternal soluble fms-like tyrosine kinase 1 (P=0.05) and high-sensitivity C-reactive protein (P=0.02) were elevated in the preeclampsia group compared with controls. High concentrations of these maternal biomarkers both at delivery and 5 to 8 years postpartum were also more frequent in preeclampsia compared with controls (P<0.05). The novelty of our study is the parallel finding of reduced endothelial function in mother and child pairs 5 to 8 years after small-for-gestational-age preeclamptic pregnancies, accompanied by increased inflammatory and antiangiogenic maternal biomarkers. This finding supports the concept of transgenerational risk of cardiovascular disease after preeclampsia.
子痫前期是母亲长期心血管风险因素，可能对子代也有影响。子痫前期和心血管疾病具有共同的病理生理特征，包括内皮功能障碍。我们探讨了在分娩后 5 至 8 年，是否存在非侵入性测量的内皮功能以及反映脂质代谢、血管生成和炎症的循环生物标志物存在差异，这些差异存在于伴有子痫前期的母亲和后代配对与无复杂妊娠的母亲和后代配对中。26 对伴有子痫前期的母亲和孩子与 17 对无复杂妊娠的母亲和孩子进行了比较。此外，我们评估了分娩时母体循环生物标志物的浓度是否可以预测产后 5 至 8 年的结果。我们还评估了早发型子痫前期，并特别关注了小于胎龄儿的影响。与无小于胎龄儿的妊娠相比，伴有小于胎龄儿的子痫前期母亲和孩子的内皮功能均显著降低（母亲：P<0.001；孩子：P<0.05）。与对照组相比，子痫前期组产后母亲可溶性 fms 样酪氨酸激酶 1（P=0.05）和高敏 C 反应蛋白（P=0.02）升高。分娩时和产后 5 至 8 年时母体这些生物标志物的高浓度在子痫前期中也比对照组更常见（P<0.05）。我们研究的新颖之处在于，在伴有小于胎龄儿的子痫前期母亲和孩子中，在分娩后 5 至 8 年发现内皮功能降低，同时伴有炎症和抗血管生成的母体生物标志物增加。这一发现支持了子痫前期后心血管疾病存在跨代风险的概念。
