From the Department of Psychiatry (Brindle, Duggan, Hall), University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Psychological Sciences (Cribbet), Texas Tech University, Lubbock, Texas; Departments of Health and Physical Activity (Kline) and Biostatistics (Krafty), University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Psychology (Thayer), Ohio State University, Columbus, Ohio; and Department of Medicine (Mulukutla), University of Pittsburgh, Pittsburgh, Pennsylvania.
Psychosom Med. 2018 Apr;80(3):301-306. doi: 10.1097/PSY.0000000000000560.
Exaggerated cardiovascular reactivity to acute psychological stress has been associated with increased carotid intima-media thickness (IMT). However, interstudy variability in this relationship suggests the presence of moderating factors. The current study aimed to test the hypothesis that poor nocturnal sleep, defined as short total sleep time or low slow-wave sleep, would moderate the relationship between cardiovascular reactivity and IMT.
Participants (N = 99, 65.7% female, age = 59.3 ± 9.3 years) completed a two-night laboratory sleep study and cardiovascular examination where sleep and IMT were measured. The multisource interference task was used to induce acute psychological stress, while systolic and diastolic blood pressure and heart rate were monitored. Moderation was tested using the PROCESS framework in SPSS.
Slow-wave sleep significantly moderated the relationship between all cardiovascular stress reactivity variables and IMT (all pinteraction ≤ .048, all ΔRinteraction ≥ .027). Greater stress reactivity was associated with higher IMT values in the low slow-wave sleep group and lower IMT values in the high slow-wave sleep group. No moderating effects of total sleep time were observed.
The results provide evidence that nocturnal slow-wave sleep moderates the relationship between cardiovascular stress reactivity and IMT and may buffer the effect of daytime stress-related disease processes.
急性心理应激下心血管反应过度与颈动脉内膜中层厚度(IMT)增加有关。然而,这种关系在不同研究中的可变性表明存在调节因素。本研究旨在检验以下假设,即定义为总睡眠时间短或慢波睡眠低的较差夜间睡眠会调节心血管反应性与 IMT 之间的关系。
99 名参与者(65.7%为女性,年龄=59.3±9.3 岁)完成了两晚的实验室睡眠研究和心血管检查,其中测量了睡眠和 IMT。多源干扰任务用于诱发急性心理应激,同时监测收缩压、舒张压和心率。使用 SPSS 中的 PROCESS 框架检验调节作用。
慢波睡眠显著调节了所有心血管应激反应变量与 IMT 之间的关系(所有 p 交互作用值均≤.048,所有 ΔR 交互作用值均≥.027)。在慢波睡眠较低的组中,较高的应激反应与较高的 IMT 值相关,而在慢波睡眠较高的组中,较低的 IMT 值与较高的应激反应相关。未观察到总睡眠时间的调节作用。
结果提供了证据表明,夜间慢波睡眠调节了心血管应激反应性与 IMT 之间的关系,并可能缓冲日间应激相关疾病过程的影响。