von Känel, Roland; Meister-Langraf, Rebecca E; Fux, Michaela; Imholz, Laurin; Pazhenkottil, Aju P; Znoj, Hansjörg; Schmid, Jean-Paul; Zuccarella-Hackl, Claudia; Barth, Jürgen; Schnyder, Ulrich; Princip, Mary (2022). Prospective association between pro-inflammatory state on admission and posttraumatic stress following acute coronary syndrome. General hospital psychiatry, 74, pp. 58-64. Elsevier 10.1016/j.genhosppsych.2021.12.003
|
Text
vonK_nel_GenHospPsychiatry_2021.pdf - Published Version Available under License Creative Commons: Attribution (CC-BY). Download (540kB) | Preview |
OBJECTIVE
The traumatic experience of acute coronary syndrome (ACS) may induce symptoms of posttraumatic stress disorder (PTSD). We examined whether the ACS-triggered acute inflammatory response predicts the development of PTSD symptoms.
METHOD
Study participants were 70 patients (all Caucasian, 80% male, mean age 59 years) with myocardial infarction (MI) during the acute treatment phase. Interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, IL-4, IL-10, and transforming growth factor (TGF)-1β were determined in plasma collected within 48 h of hospital admission. Participants self-assessed the severity of ACS-induced PTSD symptoms with the 17-item Posttraumatic Diagnostic Scale at 12 months.
RESULTS
There was a significant positive association of the pro-inflammatory index (added standardized z-scores of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α) with total PTSD symptom severity (ΔR2 = 0.050, p = .029) and re-experiencing symptoms (ΔR2 = 0.088, p = .008), but not avoidance/numbing and hyperarousal symptoms. Analyses were adjusted for the anti-inflammatory index (added standardized z-scores of IL-4, IL-10, and TGF-β1), trauma-focused counseling, sex, age, time since pain onset, troponin, body mass index, and distress during MI. Results were robust when the anti-inflammatory index was removed from the model. Additional analyses showed significant associations of both the net-inflammatory index (i.e., pro-inflammatory index minus anti-inflammatory index) and IL-1β with total PTSD symptom severity, re-experiencing, and hyperarousal symptoms (ΔR2 between 0.042 and 0.090) and of IL-1β with avoidance/numbing symptoms (ΔR2 = 0.050).
CONCLUSIONS
The findings suggest an association between the pro-inflammatory state launched during ACS and the development of PTSD symptoms. Increased IL-1β may play a particular role in the pathophysiology of ACS-induced PTSD symptoms.