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

Roland Von Känel,Rebecca E Meister-Langraf,Michaela Fux,Laurin Imholz,Aju P Pazhenkottil,Hansjörg Znoj,Jean-Paul Schmid,Claudia Zuccarella-Hackl,Jürgen Barth,Ulrich Schnyder,Mary Princip

doi:10.1016/j.genhosppsych.2021.12.003

Abstract

ObjectiveThe 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. MethodStudy 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. ResultsThere 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). ConclusionsThe 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.

Highlights

Posttraumatic stress disorder (PTSD) is a debilitating mental health condition, which can be triggered by life-threatening diseases like acute coronary syndromes (ACS) [1]
The primary aim of the myocardial infarction (MI)-SPRINT trial was to investi gate the hypothesis that the development of ACS-induced PTSD symp toms could be prevented by a one-session intervention of traumafocused counseling delivered to patients within 48 h of hospital admis sion, which could not be confirmed [17,18]
This study showed that a pro-inflammatory state resulting from the ACS-triggered systemic inflammatory response within 48 h of hospital ization is associated with ACS-induced total severity of PTSD symptoms 12 months later

Summary

Introduction

Posttraumatic stress disorder (PTSD) is a debilitating mental health condition, which can be triggered by life-threatening diseases like acute coronary syndromes (ACS) [1]. ACSinduced PTSD symptoms are associated with poor quality of life and an increased risk of adverse outcomes, including recurrent cardiac events and premature mortality [2]. Stress doses of hydrocortisone before induction of anesthesia and on three postoperative days in patients undergoing cardiac surgery resulted in less 6-month total PTSD symptoms than placebo [5]. In another placebocontrolled study in cardiac surgery patients, a single dose of dexa methasone administered after induction of anesthesia was associated with a lower risk of severe PTSD symptomatology after a median followup of 33 months in women but not in men [6]

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