Kovell Lara C, Denu Mawulorm K I, Berkowitz Julia, Shankara Sravya, Shao Cassie, Skaritanov Ekaterina, Wilkie Gianna, Simas Tiffany A Moore, Juraschek Stephen P
Division of Cardiovascular Medicine, Department of Medicine, UMass Chan Medical School, Worcester, Massachusetts, USA.
Department of Obstetrics and Gynecology, UMass Chan Medical School/UMass Memorial Health, Worcester, Massachusetts, USA.
Am J Hypertens. 2025 Aug 14;38(9):697-705. doi: 10.1093/ajh/hpaf061.
Mechanisms of injury due to hypertension (HTN) in pregnancy remain poorly characterized. This study examined trends in markers of cardiac injury (high-sensitivity troponin I, hs-cTnI), strain (N-terminal pro-B-type natriuretic peptide, NT-proBNP), and inflammation (high-sensitivity C-reactive protein, hs-CRP) in pregnancies with and without HTN.
This prospective, 1:1 case-control study enrolled pregnant women with and without HTN (24-32 weeks gestation) from 2019 to 2022. HTN was defined by a clinical diagnosis of HTN or baseline blood pressure (BP) ≥ 140/90 mm Hg. Serum was collected at baseline, predelivery, and postpartum day 1. Mixed effects tobit models compared log-transformed hs-cTnI, NT-proBNP, and hs-CRP across HTN groups and over time, adjusted for age and body mass index.
Mean baseline BP was 130.5 (17.5)/88.2 (13.5) mm Hg for the HTN group (n = 38, 86.8% chronic, 13.2% gestational HTN), and 112.0 (9.8)/70.9 (8.2) mm Hg for those without HTN (n = 38). Over pregnancy, the HTN group had higher hs-cTnI than those without HTN (2.12 [0.43] vs. 1.07 [0.25], Δ1.05 [95%CI: 0.07-2.03] ng/l). Compared to baseline, hs-cTnI increased at predelivery and postpartum for both groups. Overall, the two groups had similar NT-proBNP (HTN: 39.0 [4.5] vs. no HTN: 35.6 [4.3] pg/mL) and hs-CRP (HTN: 12.0 [1.7] vs. no HTN: 9.9 [1.5] mg/L). For both groups, NT-proBNP and hs-CRP increased from baseline to postpartum (NT-proBNP, HTN: 127% [58-227%], no HTN: 120% [51-219%]; hs-CRP: HTN: 550% [343-853%], no HTN: 664% [415-1,034%]).
HTN was associated with markers of cardiac injury during pregnancy, while delivery alone led to increases in markers of strain and inflammation. These biomarker changes associated with HTN in pregnancy may represent potential mechanisms to explain adverse cardiovascular events.
妊娠期高血压（HTN）导致损伤的机制仍未得到充分描述。本研究调查了有和没有HTN的妊娠中心脏损伤标志物（高敏肌钙蛋白I，hs-cTnI）、应变标志物（N末端B型利钠肽原，NT-proBNP）和炎症标志物（高敏C反应蛋白，hs-CRP）的变化趋势。
这项前瞻性1:1病例对照研究纳入了2019年至2022年患有和未患有HTN（妊娠24-32周）的孕妇。HTN通过HTN的临床诊断或基线血压（BP）≥140/90 mmHg来定义。在基线、分娩前和产后第1天采集血清。混合效应 Tobit模型比较了HTN组之间以及随时间变化的对数转换后的hs-cTnI、NT-proBNP和hs-CRP，并对年龄和体重指数进行了调整。
HTN组（n = 38，86.8%为慢性，13.2%为妊娠期HTN）的平均基线BP为130.5（17.5）/88.2（13.5）mmHg，无HTN组（n = 38）为112.0（9.8）/70.9（8.2）mmHg。在整个孕期，HTN组的hs-cTnI高于无HTN组（2.12 [0.43] vs. 1.07 [0.25]，差值1.05 [95%CI：0.07-2.03] ng/l）。与基线相比，两组的hs-cTnI在分娩前和产后均升高。总体而言，两组的NT-proBNP（HTN组：39.0 [4.5] vs. 无HTN组：35.6 [4.3] pg/mL）和hs-CRP（HTN组：12.0 [1.7] vs. 无HTN组：9.9 [1.5] mg/L）相似。对于两组，NT-proBNP和hs-CRP从基线到产后均升高（NT-proBNP，HTN组：127% [58-227%]，无HTN组：120% [51-219%]；hs-CRP：HTN组：550% [343-853%]，无HTN组：664% [415-1,034%]）。
HTN与妊娠期心脏损伤标志物相关，而仅分娩就导致应变和炎症标志物增加。这些与妊娠期HTN相关的生物标志物变化可能代表了解释不良心血管事件的潜在机制。
