Examining the Crux of Autonomic Dysfunction in Posttraumatic Stress Disorder: Whether Chronic or Situational Distress Underlies Elevated Heart Rate and Attenuated Heart Rate Variability.
Examining the Crux of Autonomic Dysfunction in Posttraumatic Stress Disorder: Whether Chronic or Situational Distress Underlies Elevated Heart Rate and Attenuated Heart Rate Variability.
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DOI：
10.1097/psy.0000000000000326
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发表时间：
2016-09
影响因子：
3.3
通讯作者：
Beckham JC
中科院分区：
文献类型：
--
作者：
Dennis PA;Dedert EA;Van Voorhees EE;Watkins LL;Hayano J;Calhoun PS;Sherwood A;Dennis MF;Beckham JC
在横断面研究中，创伤后应激障碍（PTSD）与心率（HR）升高和心率变异性（HRV）降低有关。使用生态瞬时评估（EMA）和分钟到分钟的HRV/HR监测，我们检查是否PTSD症状严重程度和HRV/HR之间的横断面关联是由于整体水平的升高，在急性痛苦发作或衰减自主调节。219名年轻人（18-39岁），99名患有PTSD，接受了一天的霍尔特监测，同时通过EMA报告了痛苦水平。使用多层次模型，我们研究了短暂的痛苦和5分钟的手段，低频（LF）和高频（HF）HRV和HR紧接着痛苦评级之间的关联，以及PTSD症状的严重程度是否缓和这些协会。与对照组相比，患有PTSD的参与者记录了更高的行走痛苦（M=1.7±SD=0.5 vs. 1.2±0.3，p < .001）和HR（87.2±11.8 vs. 82.9±12.6 bpm，p = 0.011）和较低的动态LF HRV（36.9±14.7 vs. 43.7±16.9 ms，p = .002）和HF HRV（22.6±12.3 vs. 26.4±14.6 ms，p = .043）。总体痛苦水平不能预测HR或HRV（ps > 0.27）。然而，基线PTSD症状严重程度与急性短暂性痛苦反应的HR升高相关，t（1257）= 2.76，p = 0.006，LF减弱，t（1257）=-3.86，p <0.001，HF减弱，t（1257）=-2.62，p = 0.009。结果表明，创伤后应激障碍与情境痛苦后的高度觉醒有关，并可以解释先前的研究结果将创伤后应激障碍与HR/HRV联系起来。治疗和心血管风险的影响进行了讨论。
Posttraumatic stress disorder (PTSD) has been linked to elevated heart rate (HR) and reduced heart-rate variability (HRV) in cross-sectional research. Using ecological momentary assessment (EMA) and minute-to-minute HRV/HR monitoring, we examined whether cross-sectional associations between PTSD symptom severity and HRV/HR were due to overall elevations in distress levels or to attenuated autonomic regulation during episodes of acute distress. Two hundred nineteen young adults (18–39 years old), 99 with PTSD, underwent one day of Holter monitoring and concurrently reported distress levels via EMA. Using multilevel modeling, we examined the associations between momentary distress and the 5-minute means for low-frequency (LF) and high-frequency (HF) HRV and HR immediately following distress ratings, and whether PTSD symptom severity moderated these associations. Compared to controls, participants with PTSD recorded higher ambulatory distress (M=1.7±SD=0.5 vs. 1.2±0.3, p < .001) and HR (87.2±11.8 vs. 82.9±12.6 bpm, p = .011), and lower ambulatory LF HRV (36.9±14.7 vs. 43.7±16.9 ms, p = .002) and HF HRV (22.6±12.3 vs. 26.4±14.6 ms, p = .043). Overall distress level was not predictive of HR or HRV (ps > .27). However, baseline PTSD symptom severity was associated with elevated HR, t(1257) = 2.76, p = .006, and attenuated LF, t(1257) = −3.86, p < .001, and HF, t(1257) = −2.62, p = .009, in response to acute momentary distress. Results suggest that PTSD is associated with heightened arousal following situational distress and could explain prior findings associating PTSD with HR/HRV. Implications for treatment and cardiovascular risk are discussed.