Preeclampsia, a multisystem pregnancy-specific hypertensive disorder, results in significant maternal and perinatal morbidity and mortality. This condition is associated with placental histopathological abnormalities and particularly affects the decidual spiral arteries. Reportedly, aspirin prevents preeclampsia, specifically early-onset preeclampsia, although findings in decidual arteries in women treated with aspirin therapy remain unclear. We compared the clinical and histopathological placental findings between women with a history of preeclampsia, who did and did not receive low-dose aspirin therapy (LDA and non-LDA groups, respectively). We identified 26 women with a history of preeclampsia; 9 women received LDA (aspirin ≤ 100 mg/day, initiated at < 16 weeks, LDA group), and 17 women did not receive LDA (non-LDA group). The mean gestational age was higher (36.7 weeks vs. 32.3 weeks, P = 0.0221) and the incidence of preeclampsia was lower (11% vs. 59%, P = 0.0362) in the LDA than in the non-LDA group. Histopathologically, the incidence of decidual arteriopathy, particularly that of fibrinoid necrosis and thrombosis, was lower in the LDA than in the non-LDA group (44% vs. 88%, P = 0.0283). Immunohistologically, endothelial marker (CD31 and CD39) expression was stronger in the LDA than in the non-LDA group. Notably, we observed no significant intergroup differences in inflammatory changes (chronic perivasculitis, protease-activated receptor 1 expression, and CD3-positive cells). This study highlights that LDA inhibits hypertension-induced endothelial injury and thrombosis, and thereby protects maternal placental perfusion and prevents preeclampsia.

先兆子痫是一种多系统妊娠特异性高血压疾病，会导致显着的孕产妇和围产期发病率和死亡率。这种情况与胎盘组织病理学异常有关，尤其影响蜕膜螺旋动脉。据报道，阿司匹林可预防先兆子痫，特别是早发性先兆子痫，尽管在接受阿司匹林治疗的女性蜕膜动脉中的发现仍不清楚。我们比较了接受和未接受低剂量阿司匹林治疗（分别为 LDA 组和非 LDA 组）的有先兆子痫病史的女性之间的临床和组织病理学胎盘检查结果。我们确定了 26 名有先兆子痫病史的女性；9 名女性接受了 LDA（阿司匹林 ≤ 100 mg/天，在 < 16 周开始，LDA 组），17 名女性未接受 LDA（非 LDA 组）。P  = 0.0221），LDA 组的先兆子痫发生率低于 非 LDA 组（11% 对 59%， P = 0.0362）。组织病理学上，LDA 组蜕膜动脉病变，尤其是纤维素样坏死和血栓形成的发生率低于非 LDA 组（44% 对 88%，P  = 0.0283）。免疫组织学上，LDA 组的内皮标志物（CD31 和 CD39）表达强于非 LDA 组。值得注意的是，我们没有观察到炎症变化（慢性血管周围炎、蛋白酶激活受体 1 表达和 CD3 阳性细胞）的显着组间差异。该研究强调 LDA 可抑制高血压引起的内皮损伤和血栓形成，从而保护母体胎盘灌注并预防先兆子痫。