Cardiovascular Health and Autonomic Regulation Laboratory, Department of Kinesiology and Physical Education, McGill University, Montreal, Quebec, Canada.
McGill Research Centre for Physical Activity and Health, McGill University, Montreal, Quebec, Canada.
Am J Physiol Heart Circ Physiol. 2020 Mar 1;318(3):H581-H589. doi: 10.1152/ajpheart.00578.2019. Epub 2020 Jan 31.
Preeclampsia is associated with the development of cardiovascular diseases later in life. To investigate this phenomenon, we compared established markers of cardiovascular dysregulation between previously preeclamptic women (PPE; = 12, 13 ± 6 mo postpartum, 34 ± 6 yr) and women who had previously had an uncomplicated pregnancy [control (CTRL); = 12, 15 ± 4 mo postpartum; 29 ± 3 yr]. We hypothesized that PPE would present with elevated arterial stiffness (assessed as central and peripheral pulse wave velocity) and muscle sympathetic nerve activity (MSNA; microneurography) and blunted baroreflex sensitivity (BRS) relative to CTRL. Blood pressure (Finometer) was similar between PPE and CTRL (mean arterial pressure: 94 ± 11 vs. 89 ± 9, = 0.16). Central (6.92 ± 0.21 vs. 6.24 ± 0.22 m/s, = 0.04) but not peripheral arterial stiffness (7.52 ± 0.19 vs. 7.09 ± 0.19 m/s, = 0.13) was elevated in PPE versus CTRL (values normalized to MAP). MSNA was also elevated in PPE versus CTRL (22 ± 7 vs. 13 ± 5 bursts/min, = 0.01), although this was independent of arterial stiffness (central: = 0.01, = 0.74; peripheral: = 0.01, = 0.74). Cardiovagal BRS was blunted in PPE versus CTRL (15 ± 5 vs. 28 ± 1 ms/mmHg, = 0.01), whereas sympathetic vascular BRS was similar (-3.2 ± 0.9 vs. -3.1 ± 1.4 bursts·100 hb·mmHg, 0.88). Cardiovagal and sympathetic BRS were inversely correlated in both CTRL ( = 0.43; = 0.05) and PPE ( = 0.69; = 0.04), supporting a compensatory mechanism resulting in normal blood pressures in both groups. Overall, these data indicate that PPE retain their ability to buffer elevated MSNA. We propose that the higher incidence of cardiovascular disease observed later in life in PPE results from this arterial stiffness, combined with the loss of protective vascular mechanisms and the "unmasking" of high MSNA. We demonstrate that resting muscle sympathetic nerve activity is elevated in women with a recent history of preeclampsia relative to women who have recently had uncomplicated pregnancies and without a history of preeclampsia. Structural changes in the central arteries are associated with arterial stiffness following preeclampsia, independent of changes in the sympathetic nervous system. The structural changes are observed in these relatively young previously preeclamptic women, indicating elevated cardiovascular risk. Our data suggest that with aging (and the gradual loss of vascular protection for women, as established by others), this risk will become exaggerated compared with women who have had normal pregnancies.
子痫前期与生命后期心血管疾病的发展有关。为了研究这一现象,我们比较了先前患有子痫前期的妇女(PPE;= 12,产后 13 ± 6 个月,34 ± 6 岁)和先前有过正常妊娠的妇女(CTRL;= 12,产后 15 ± 4 个月;29 ± 3 岁)中已确立的心血管调节障碍标志物。我们假设 PPE 会表现出较高的动脉僵硬(评估为中心和外周脉搏波速度)和肌肉交感神经活动(微神经记录),以及血压调节反射敏感性(BRS)降低,与 CTRL 相比。PPE 和 CTRL 的血压(Finometer)相似(平均动脉压:94 ± 11 对 89 ± 9,= 0.16)。与 CTRL 相比,PPE 中的中心动脉僵硬(6.92 ± 0.21 对 6.24 ± 0.22 m/s,= 0.04)但不是外周动脉僵硬(7.52 ± 0.19 对 7.09 ± 0.19 m/s,= 0.13)升高(将值归一化为 MAP)。与 CTRL 相比,PPE 中的 MSNA 也升高(22 ± 7 对 13 ± 5 个爆发/分钟,= 0.01),尽管这与动脉僵硬无关(中心:= 0.01,= 0.74;外周:= 0.01,= 0.74)。与 CTRL 相比,PPE 中的迷走神经 BRS 降低(15 ± 5 对 28 ± 1 ms/mmHg,= 0.01),而交感血管 BRS 相似(-3.2 ± 0.9 对 -3.1 ± 1.4 爆发·100 hb·mmHg,= 0.88)。在 CTRL(= 0.43;= 0.05)和 PPE(= 0.69;= 0.04)中,迷走神经和交感神经 BRS 呈负相关,支持两组正常血压的代偿机制。总的来说,这些数据表明 PPE 保留了缓冲升高的 MSNA 的能力。我们提出,PPE 中观察到的生命后期心血管疾病发生率较高的原因是动脉僵硬,加上血管保护机制的丧失和高 MSNA 的“暴露”。我们证明,与近期有正常妊娠史且无子痫前期史的妇女相比,近期有子痫前期史的妇女静息肌肉交感神经活动升高。子痫前期后中枢动脉的结构变化与动脉僵硬有关,与交感神经系统的变化无关。这些结构变化在这些相对年轻的先前患有子痫前期的妇女中观察到,表明心血管风险升高。我们的数据表明,随着年龄的增长(以及其他人所建立的女性血管保护的逐渐丧失),与有正常妊娠史的女性相比,这种风险将变得更加突出。