Cortisol, heart rate, and blood pressure as early markers of PTSD risk: A systematic review and meta-analysis.

Cortisol, heart rate, and blood pressure as early markers of PTSD risk: A systematic review and meta-analysis.
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皮质醇,心率和血压作为PTSD风险的早期标记:系统的综述和荟萃分析。

DOI:
10.1016/j.cpr.2016.09.001
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发表时间:
2016-11
影响因子:
12.8
通讯作者:
Rao, Uma
Rao, Uma
中科院分区:
心理学1区
文献类型:
--
作者:
Morris, Matthew C.;Hellman, Natalie;Abelson, James L.;Rao, Uma

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患有创伤后应激障碍(PTSD)的个体通常表现出改变的下丘脑-垂体-肾上腺(HPA)功能和交感神经系统(SNS)活动。本研究的目的是确定是否HPA和SNS的改变在创伤后立即预测随后的PTSD症状的发展,以及是否研究之间观察到的不一致可以解释关键的人口统计学和方法学因素。这项工作通过识别创伤幸存者中有患创伤后应激障碍风险的亚组,为创伤后应激障碍的二级预防提供信息。这项荟萃分析(26项研究,N = 5,186人)显示,创伤暴露后不久测量的较高心率与随后较高的PTSD症状相关(r = 0.13)。皮质醇(r =-0.07)和血压(舒张压:r =-0.01;收缩压:r = 0.02)都与PTSD症状无关,这可能受到方法学限制的影响。风险标志物(心率,皮质醇,收缩压)和PTSD症状之间的关联在年轻样本中是正向的,在老年样本中是负向的。这些发现通过揭示早期风险标志物呈现的年龄相关变化,扩展了PTSD的发展创伤学模型。需要做更多的工作来确定创伤后应激障碍的风险标志和途径,同时解决方法上的局限性,以便制定和针对预防性干预措施。
Individuals with posttraumatic stress disorder (PTSD) typically exhibit altered hypothalamic-pituitary-adrenal (HPA) function and sympathetic nervous system (SNS) activity. The goals of this study were to determine whether HPA and SNS alterations in the immediate aftermath of trauma predict subsequent PTSD symptom development and whether inconsistencies observed between studies can be explained by key demographic and methodological factors. This work informs secondary prevention of PTSD by identifying subgroups of trauma survivors at risk for PTSD. This meta-analysis (26 studies, N = 5,186 individuals) revealed that higher heart rate measured soon after trauma exposure was associated with higher PTSD symptoms subsequently (r = .13). Neither cortisol (r = −.07) nor blood pressure (diastolic: r = −.01; systolic: r = .02) were associated with PTSD symptoms which may be influenced by methodological limitations. Associations between risk markers (heart rate, cortisol, systolic blood pressure) and PTSD symptoms were in the positive direction for younger samples and negative direction for older samples. These findings extend developmental traumatology models of PTSD by revealing an age-related shift in the presentation of early risk markers. More work will be needed to identify risk markers and pathways to PTSD while addressing methodological limitations in order to shape and target preventive interventions.
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