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Prospective association between pro-inflammatory state on admission and posttraumatic stress following acute coronary syndrome


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, 74:58-64.

Abstract

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 symp-toms. 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.

Abstract

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 symp-toms. 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.

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Complementary Medicine
04 Faculty of Medicine > Psychiatric University Hospital Zurich > Clinic for Psychiatry, Psychotherapy, and Psychosomatics
04 Faculty of Medicine > University Hospital Zurich > Klinik für Konsiliarpsychiatrie und Psychosomatik
04 Faculty of Medicine > University Hospital Zurich > Clinic for Cardiology
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Psychiatry and Mental Health
Uncontrolled Keywords:Cardiovascular disease; Cytokines; Inflammation; Longitudinal study; Psychological stress; Trauma
Language:English
Date:1 January 2022
Deposited On:27 Dec 2021 06:02
Last Modified:27 May 2024 01:46
Publisher:Elsevier
ISSN:0163-8343
OA Status:Hybrid
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.genhosppsych.2021.12.003
PubMed ID:34915233
Project Information:
  • : FunderSNSF
  • : Grant ID32003B_140960
  • : Project TitleA Randomized-Controlled Minimal Early Behavioral Intervention Trial to Prevent the Development of Posttraumatic Stress Caused by Acute Myocardial Infarction
  • Content: Published Version
  • Language: English
  • Licence: Creative Commons: Attribution 4.0 International (CC BY 4.0)