Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA.
Hypertens Res. 2018 Apr;41(4):282-289. doi: 10.1038/s41440-018-0017-5. Epub 2018 Feb 15.
Endothelial dysfunction is a form of subclinical cardiovascular disease that may be involved in preterm birth and small-for-gestational-age deliveries. However, concentrations of biomarkers of endothelial dysfunction before pregnancy have rarely been measured. We hypothesized that higher levels of biomarkers of endothelial dysfunction (cellular adhesion molecules and selectins) would be associated with odds of preterm birth and/or small-for-gestational-age deliveries. We included 235 women from the Coronary Artery Risk Development in Young Adults (CARDIA) study who were nulliparous at Y7, reported ≥1 live birth through Y25, and had ≥1 biomarker measured at Y7. We tested for associations between individual biomarkers and an averaged z-score representing total endothelial dysfunction with preterm birth and/or small-for-gestational-age deliveries using Poisson regression, adjusted for demographic and clinical characteristics at the exam immediately preceding index birth. At Y7, total evidence of endothelial dysfunction was similar in women who did (n = 59) and did not have (n = 176) preterm birth and/or small-for-gestational-age deliveries. There was no association between biomarkers of endothelial dysfunction (either individual biomarker or total score) with odds of preterm birth and/or small-for-gestational-age deliveries after adjustment: IRR = 1.01, 95% CI: 0.74, 1.39, p = 0.93 for total endothelial biomarker score. Associations were not modified by race. We conclude that biomarkers of endothelial dysfunction in nulliparous women, measured ~3 years before pregnancy, did not identify women at risk for preterm birth and/or small-for-gestational-age deliveries. This suggests that the maternal endothelial dysfunction that is believed to contribute to these birth outcomes may not be detectable before pregnancy.
内皮功能障碍是一种亚临床心血管疾病,可能与早产和胎儿生长受限有关。然而,妊娠前内皮功能障碍生物标志物的浓度很少被测量。我们假设,更高水平的内皮功能障碍生物标志物(细胞黏附分子和选择素)与早产和/或胎儿生长受限的几率相关。我们纳入了来自冠状动脉风险发展在年轻人(CARDIA)研究的 235 名初产妇,她们在 Y7 时为初产妇,在 Y25 时报告了≥1 次活产,并且在 Y7 时至少有 1 项生物标志物被测量。我们使用泊松回归测试了个体生物标志物与平均 z 分数(代表总内皮功能障碍)与早产和/或胎儿生长受限之间的关联,该平均 z 分数是在指数分娩前的检查中根据人口统计学和临床特征进行调整的。在 Y7 时,有早产和/或胎儿生长受限的女性(n=59)与没有早产和/或胎儿生长受限的女性(n=176)之间,总内皮功能障碍的证据相似。在调整后,内皮功能障碍生物标志物(单个生物标志物或总评分)与早产和/或胎儿生长受限的几率之间没有关联:IRR=1.01,95%CI:0.74,1.39,p=0.93 对于总内皮生物标志物评分。种族因素并未改变这种关联。我们得出结论,在妊娠前约 3 年测量的初产妇内皮功能障碍生物标志物不能识别有早产和/或胎儿生长受限风险的女性。这表明,被认为导致这些分娩结局的母体内皮功能障碍可能在妊娠前无法检测到。