Department of Biomedical Informatics, School of Medicine, Emory University, Atlanta, Georgia, USA.
Department of Health Sciences and Technology, ETH Zürich, Zürich, Switzerland.
Psychophysiology. 2023 Feb;60(2):e14167. doi: 10.1111/psyp.14167. Epub 2022 Aug 12.
Post-traumatic stress disorder (PTSD) has been associated with cardiovascular disease (CVD), but the mechanisms remain unclear. Autonomic dysfunction, associated with higher CVD risk, may be triggered by acute PTSD symptoms. We hypothesized that a laboratory-based trauma reminder challenge, which induces acute PTSD symptoms, provokes autonomic dysfunction in a cohort of veteran twins. We investigated PTSD-associated real-time physiologic changes with a simulation of traumatic experiences in which the twins listened to audio recordings of a one-minute neutral script followed by a one-minute trauma script. We examined two heart rate variability metrics: deceleration capacity (DC) and logarithmic low frequency (log-LF) power from beat-to-beat intervals extracted from ambulatory electrocardiograms. We assessed longitudinal PTSD status with a structured clinical interview and the severity with the PTSD Symptoms Scale. We used linear mixed-effects models to examine twin dyads and account for cardiovascular and behavioral risk factors. We examined 238 male Veteran twins (age 68 ± 3 years old, 4% black). PTSD status and acute PTSD symptom severity were not associated with DC or log-LF measured during the neutral session, but were significantly associated with lower DC and log-LF during the traumatic script listening session. Long-standing PTSD was associated with a 0.38 (95% confidence interval, -0.83,-0.08) and 0.79 (-1.30,-0.29) standardized unit lower DC and log-LF, respectively, compared to no history of PTSD. Traumatic reminders in patients with PTSD lead to real-time autonomic dysregulation and suggest a potential causal mechanism for increased CVD risk, based on the well-known relationships between autonomic dysfunction and CVD mortality.
创伤后应激障碍（PTSD）与心血管疾病（CVD）有关，但机制尚不清楚。自主神经功能障碍与更高的 CVD 风险相关，可能是由急性 PTSD 症状引发的。我们假设，一项基于实验室的创伤提醒挑战，可诱发急性 PTSD 症状，会在一组退伍军人双胞胎中引发自主神经功能障碍。我们通过模拟创伤经历来研究与 PTSD 相关的实时生理变化，双胞胎在该模拟中听一分钟中性脚本的录音，然后听一分钟创伤脚本的录音。我们检查了两种心率变异性指标：减速能力（DC）和从动态心电图的心跳间隔中提取的对数低频（log-LF）功率。我们使用结构临床访谈评估纵向 PTSD 状态，并使用 PTSD 症状量表评估严重程度。我们使用线性混合效应模型来检查双胞胎对子，并考虑心血管和行为风险因素。我们检查了 238 名男性退伍军人双胞胎（年龄 68±3 岁，4%为黑人）。PTSD 状态和急性 PTSD 症状严重程度与中性会话期间的 DC 或 log-LF 无关，但与创伤脚本收听会话期间的 DC 和 log-LF 显著相关。长期 PTSD 与 DC 降低 0.38（95%置信区间，-0.83，-0.08）和 log-LF 降低 0.79（-1.30，-0.29）标准化单位相关，与无 PTSD 史相比。PTSD 患者的创伤提醒会导致实时自主神经调节紊乱，并基于自主神经功能障碍与 CVD 死亡率之间的已知关系，提示增加 CVD 风险的潜在因果机制。
