Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Department of Obstetrics & Gynaecology, Queen's University, Kingston, Ontario, Canada.
Am J Physiol Heart Circ Physiol. 2021 Apr 1;320(4):H1393-H1402. doi: 10.1152/ajpheart.00767.2020. Epub 2021 Jan 22.
Preeclampsia is associated with adverse maternal health outcomes later in life. Vascular endothelial dysfunction has been previously described following preeclampsia. We hypothesized that microvascular endothelial dysfunction associated with preeclampsia persists postpartum and may identify those at greatest risk of future cardiovascular disease. The objective of this study was to examine postpartum microvascular endothelial function in women after a pregnancy complicated by preeclampsia. Women with previous preeclampsia ( = 30) and normotensive controls ( = 30) between 6 mo and 5 yr postpartum were recruited. Severity of preeclampsia [severe ( = 16) and mild ( = 14)] was determined by standardized chart review. Microvascular reactivity in the forearm was measured with laser speckle contrast imaging, coupled with iontophoresis; endothelium-dependent and endothelium-independent vasodilation was induced with 1% acetylcholine and sodium nitroprusside solutions, respectively. A postocclusive reactive hyperemia test assessed vasodilatory response following three minutes of suprasystolic (200 mmHg) occlusion with a mechanized cuff. Women with prior severe preeclampsia exhibited significantly higher vasodilation to acetylcholine and sodium nitroprusside compared to controls ( < 0.01; = 0.03) and prior mild preeclampsia ( = 0.03; < 0.01). Neither the degree of postocclusive reactive hyperemia ( = 0.98), nor time to return halfway to baseline [OR = 1.026 (0.612, 1.72); = 0.92], differed between preeclampsia and controls. In conclusion, severe preeclampsia is associated with heightened postpartum microvascular endothelium-dependent and endothelium-independent vasoreactivity. These changes, or a common antecedent, may be linked to postpartum alterations in vascular function that predispose women to disease after preeclampsia. Further investigation should identify the contributing mechanism and the degree to which it could be amenable to medical intervention. We examine maternal microvascular function after preeclampsia, identifying heightened endothelium-dependent and endothelium-independent microvascular reactivity following severe disease. Our study represents a noteworthy addition to the existing literature with the use of a novel imaging modality, vascular perturbation, postpartum time point, and patient population with differentiation of preeclampsia into severe and nonsevere subtypes. These results represent a novel addition to the growing clinical and academic understanding of maternal health outcomes following preeclampsia.
子痫前期与母亲生命后期的不良健康结局有关。此前已描述过子痫前期后血管内皮功能障碍。我们假设与子痫前期相关的微血管内皮功能障碍在产后持续存在，并可能识别出那些未来患心血管疾病风险最大的人。本研究的目的是检查患有子痫前期的孕妇产后的微血管内皮功能。在产后 6 个月至 5 年期间，招募了患有先前子痫前期（n=30）和正常血压对照（n=30）的女性。通过标准化图表审查确定子痫前期的严重程度[重度（n=16）和轻度（n=14）]。使用激光散斑对比成像与离子电渗法测量前臂的微血管反应；分别用 1%乙酰胆碱和硝普钠溶液诱导内皮依赖性和非内皮依赖性血管舒张。用机械加压袖口进行 3 分钟的超收缩（200mmHg）闭塞后，进行闭塞后反应性充血测试，以评估血管舒张反应。与对照组相比，先前患有重度子痫前期的女性对乙酰胆碱和硝普钠的血管舒张作用明显更高（<0.01；=0.03），且与先前患有轻度子痫前期的女性相比也更高（=0.03；<0.01）。无论是闭塞后反应性充血的程度（=0.98），还是恢复到基线一半的时间[比值比（OR）=1.026（0.612，1.72）；=0.92]，子痫前期与对照组之间均无差异。总之，重度子痫前期与产后微血管内皮依赖性和非内皮依赖性血管反应性增强有关。这些变化或共同的前提条件可能与子痫前期后血管功能的产后改变有关，使女性容易患病。进一步的研究应确定促成机制及其可通过医疗干预改变的程度。我们检查了子痫前期后的产妇微血管功能，发现严重疾病后存在增强的内皮依赖性和非内皮依赖性微血管反应。我们的研究使用了一种新的成像方式、血管干扰、产后时间点和子痫前期严重和非严重亚型的患者人群，对现有文献做出了重要补充。这些结果代表了对子痫前期后产妇健康结局的不断增长的临床和学术理解的一个新的补充。
