目的:肥胖是育龄妇女最常见的健康问题,这对母婴健康产生了深远的影响。尽管在了解关键的炎症和代谢变化方面取得了进展,肥胖孕妇心血管表型的发病机制仍有待充分了解。这项研究旨在:(i)评估肥胖与正常体重(对照)妇女在整个怀孕期间肾素-血管紧张素系统(RAS)的变化,(ii)评估母体血液动力学状态与RAS变化之间是否存在任何关联。
结果:纳入了38名正常体重和19名肥胖孕妇。临床评估,在12、20、30和36周进行血液样本和母体血流动力学评估,而超声评估计划在妊娠20,30和36周进行。sFlt-1,PlGF,血管紧张素原,Renin,AngII,通过ELISA进行Ang1-7、ACE和ACE2。我们的数据显示血压正常的肥胖女性胎盘供血较少,根据UV-Q和UV-Q/EFW评估,与对照组相比,以及明显更高水平的AngII和AngII/Ang1-7比率,与胎盘血液供应成反比。
结论:我们的研究首次表明,正常血压的肥胖女性在整个怀孕期间表现出AngII和AngII/Ang1-7的显着进行性增加,通过UV-Q和UV-Q/EFW评估,这与胎盘血液供应呈负相关。我们的数据揭示了妊娠肥胖妇女的早期变化,并表明RAS失调是妊娠高血压疾病和其他母体新生儿并发症的先决条件,而不是结果。
OBJECTIVE: Obesity is the most common health issue in women of reproductive age, which profoundly affects maternal-fetal health. Despite progress in understanding key inflammatory and metabolic changes, the pathogenesis of the cardiovascular phenotype of obese pregnant women remains to be fully understood. This study aimed at: (i) evaluating the changes of the renin-angiotensin system (RAS) throughout pregnancy in obese vs normal weight (control) women, and (ii) evaluating the presence of any associations between maternal hemodynamic status and RAS changes.
RESULTS: Thirty-eight normal weight and nineteen obese pregnant women were included. Clinical assessment, blood samples and maternal hemodynamic evaluation were performed at 12, 20, 30, and 36 weeks, while ultrasound assessment was scheduled at 20, 30, and 36 weeks of gestation. Measurements of sFlt-1, PlGF, Angiotensinogen, Renin, AngII, Ang1-7, ACE and ACE2 were performed by ELISA. Our data show that normotensive obese women had lower placental blood supply, as assessed by UV-Q and UV-Q/EFW, as compared to controls, and significantly higher levels of AngII and AngII/Ang1-7 ratio, which were inversely related to placental blood supply.
CONCLUSIONS: Our study shows for the first time that normotensive obese women exhibited a significant progressive increase of AngII and AngII/Ang1-7 throughout pregnancy, which were inversely related to placental blood supply as assessed by UV-Q and UV-Q/EFW. Our data shed light on the early changes in pregnant obese women and suggest that RAS dysregulation is a prerequisite rather than a consequence of hypertensive disorders of pregnancy and other maternal neonatal complications.