Department of Obstetrics and Gynecology University of Chicago IL.
Department of Anesthesia and Critical Care University of Chicago IL.
J Am Heart Assoc. 2021 Feb;10(5):e018526. doi: 10.1161/JAHA.120.018526. Epub 2021 Feb 23.
Background Preeclampsia is a prominent risk factor for long-term development of cardiovascular disease. Although existing studies report a strong correlation between preeclampsia and heart failure, the underlying mechanisms are poorly understood. One possibility is the glycoprotein growth factor activin A. During pregnancy, elevated activin A levels are associated with impaired cardiac global longitudinal strain at 1 year, but whether these changes persist beyond 1 year is not known. We hypothesized that activin A levels would remain increased more than 1 year after a preeclamptic pregnancy and correlate with impaired cardiac function. Methods and Results To test our hypothesis, we performed echocardiograms and measured activin A levels in women approximately 10 years after an uncomplicated pregnancy (n=25) or a pregnancy complicated by preeclampsia (n=21). Compared with women with a previously normal pregnancy, women with preeclampsia had worse global longitudinal strain (-18.3% versus -21.3%, =0.001), left ventricular posterior wall thickness (0.91 mm versus 0.80 mm, =0.003), and interventricular septal thickness (0.96 mm versus 0.81 mm, =0.0002). Women with preeclampsia also had higher levels of activin A (0.52 versus 0.37 ng/mL, =0.02) and activin/follistatin-like 3 ratio (0.03 versus 0.02, =0.04). In a multivariable model, the relationship between activin A levels and worsening global longitudinal strain persisted after adjusting for age at enrollment, mean arterial pressure, race, and body mass index (=0.003). Conclusions Our findings suggest that both activin A levels and global longitudinal strain are elevated 10 years after a pregnancy complicated by preeclampsia. Future studies are needed to better understand the relationship between preeclampsia, activin A, and long-term cardiac function.
子痫前期是心血管疾病长期发展的一个显著危险因素。尽管现有研究报告子痫前期与心力衰竭之间存在很强的相关性,但潜在机制尚不清楚。一种可能性是糖蛋白生长因子激活素 A。在怀孕期间,激活素 A 水平升高与 1 年后心脏整体纵向应变受损相关,但这些变化是否持续超过 1 年尚不清楚。我们假设,在子痫前期妊娠后 1 年以上,激活素 A 水平仍会升高,并与心脏功能受损相关。
为了验证我们的假设,我们对大约 10 年前经历过一次无并发症妊娠(n=25)或妊娠合并子痫前期(n=21)的女性进行了超声心动图检查并测量了激活素 A 水平。与之前正常妊娠的女性相比,子痫前期女性的整体纵向应变更差(-18.3%比-21.3%,=0.001),左心室后壁厚度(0.91mm 比 0.80mm,=0.003)和室间隔厚度(0.96mm 比 0.81mm,=0.0002)。子痫前期女性的激活素 A 水平也更高(0.52ng/ml 比 0.37ng/ml,=0.02),激活素/卵泡抑素样 3 比值也更高(0.03ng/ml 比 0.02ng/ml,=0.04)。在多变量模型中,在校正了纳入时的年龄、平均动脉压、种族和体重指数后,激活素 A 水平与整体纵向应变恶化之间的关系仍然存在(=0.003)。
我们的研究结果表明,子痫前期后 10 年,激活素 A 水平和整体纵向应变均升高。需要进一步研究以更好地了解子痫前期、激活素 A 和长期心脏功能之间的关系。