BACKGROUND:Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk.METHODS:Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography within 4 weeks of delivery. A control group of premenopausal, nonpostpartum women was also included. Myocardial flow reserve, myocardial blood flow, and coronary vascular resistance were compared across groups. sFlt-1 (soluble fms-like tyrosine kinase receptor-1) and PlGF (placental growth factor) were measured at imaging.RESULTS:The primary cohort included 19 women with severe preeclampsia (imaged at a mean of 15.3 days postpartum), 5 with normotensive pregnancy (mean, 14.4 days postpartum), and 13 nonpostpartum female controls. Preeclampsia was associated with lower myocardial flow reserve (β, −0.67 [95% CI, −1.21 to −0.13]; P=0.016), lower stress myocardial blood flow (β, −0.68 [95% CI, −1.07 to −0.29] mL/min per g; P=0.001), and higher stress coronary vascular resistance (β, +12.4 [95% CI, 6.0 to 18.7] mm Hg/mL per min/g; P=0.001) versus nonpostpartum controls. Myocardial flow reserve and coronary vascular resistance after normotensive pregnancy were intermediate between preeclamptic and nonpostpartum groups. Following preeclampsia, myocardial flow reserve was positively associated with time following delivery (P=0.008). The sFlt-1/PlGF ratio strongly correlated with rest myocardial blood flow (r=0.71; P<0.001), independent of hemodynamics.CONCLUSIONS:In this exploratory cross-sectional study, we observed reduced coronary microvascular function in the early postpartum period following preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves coronary microcirculation. Further research is needed to establish interventions to mitigate the risk of preeclampsia-associated cardiovascular disease.

中文翻译：

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严重先兆子痫后的冠状动脉微血管功能

背景：先兆子痫是一种妊娠特异性高血压疾病，与循环促血管生成蛋白和抗血管生成蛋白失衡有关。临床前证据表明微血管功能障碍是先兆子痫相关心血管风险的潜在介质。 方法：单胎妊娠并发严重产前发作先兆子痫的妇女和正常血压分娩的对照组在分娩后 4 周内接受心脏正电子发射断层扫描。还包括绝经前、非产后妇女的对照组。比较各组之间的心肌血流储备、心肌血流量和冠状血管阻力。在成像时测量 sFlt-1（可溶性 fms 样酪氨酸激酶受体-1）和 PlGF（胎盘生长因子）。 结果：主要队列包括 19 名患有严重先兆子痫的女性（平均产后 15.3 天进行成像），其中 5 名患有严重子痫前期的女性。正常血压妊娠（平均产后 14.4 天）和 13 名非产后女性对照。先兆子痫与较低的心肌血流储备（β，-0.67 [95% CI，-1.21 至 -0.13]； P = 0.016）、较低的应激心肌血流（β，-0.68 [95% CI，-1.07 至 -0.29 ]）相关。] mL/min/g；P = 0.001），与非产后对照相比，更高的应激冠状血管阻力（β，+12.4 [95% CI，6.0 至 18.7] mm Hg/mL/min/g；P = 0.001）。正常血压妊娠后的心肌血流储备和冠状血管阻力介于先兆子痫组和非产后组之间。先兆子痫后，心肌血流储备与分娩后时间呈正相关（P =0.008）。 sFlt-1/PlGF 比值与静息心肌血流量密切相关（r =0.71；P <0.001），与血流动力学无关。 结论：在这项探索性横断面研究中，我们观察到产后早期冠状动脉微血管功能下降先兆子痫，表明先兆子痫的全身微血管功能障碍涉及冠状动脉微循环。需要进一步研究来制定干预措施来降低先兆子痫相关心血管疾病的风险。