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Gen Hosp Psychiatry. 2018 Jul - Aug;53:125-130. doi: 10.1016/j.genhosppsych.2018.03.008. Epub 2018 May 9.

C-reactive protein as a predictor of posttraumatic stress induced by acute myocardial infarction.

Author information

1
Department of Biomedical Ethics, University Hospital Zurich, University of Zurich, Zurich, Switzerland; Department of Child and Adolescent Psychosomatic Medicine, Clinic Fontane, Mittenwalde, Germany.
2
Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland; Department for BioMedical Research, University of Bern, Switzerland; Clienia Schlössli AG, Oetwil am See, Zurich, Switzerland.
3
Department of Cardiology, Clinic Barmelweid, Barmelweid, Switzerland.
4
Complementary and Integrative Medicine, University of Zurich, Zurich, Switzerland.
5
Department of Clinical Psychology and Psychotherapy, University of Bern, Switzerland.
6
University of Zurich, Zurich, Switzerland.
7
Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland; Department for BioMedical Research, University of Bern, Switzerland; Division of Cardiovascular Prevention, Rehabilitation and Sports Medicine, Department of Cardiology, Inselspital, Bern University Hospital, University of Bern, Switzerland.
8
Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland; Department for BioMedical Research, University of Bern, Switzerland; Department of Consultation-Liaison Psychiatry and Psychosomatic Medicine, University Hospital Zurich, Zurich, Switzerland. Electronic address: roland.vonkaenel@usz.ch.

Abstract

BACKGROUND:

Acute coronary syndrome (ACS) may cause clinically relevant posttraumatic stress disorder symptoms (PTSS). An inflammatory state might be one mechanism linking PTSS with poor prognosis after ACS. We tested the hypothesis that a change in C-reactive protein (CRP) between hospital admission and 3-month follow-up is an independent predictor of ACS-triggered PTSS.

METHODS:

We assessed 183 patients (median age 59 years; 84% men) with verified myocardial infarction (MI) within 48 h of an acute coronary intervention and three months post-MI for self-rated PTSS. 14 (7.7%) patients fulfilled definition criteria for PTSS caseness. CRP values were categorized according to the predicted risk of cardiovascular disease (CVD) at hospital admission (acute inflammatory response): 0 to <5 mg/L, 5 to <10 mg/L, 10 to <20 mg/L, and ≥ 20 mg/L; and at 3-month follow-up (low-grade inflammation): 0 to <1 mg/L, 1 to <3 mg/L, and ≥ 3 mg/L. Additionally, in a subsample of 84 patients with CRP levels below 20 mg/L at admission, CRP values were log-transformed.

RESULTS:

After adjustment for covariates, less of a reduction or an increase of log CRP values between admission and 3-month follow-up predicted PTSS caseness (OR 6.25, 95% CI 1.25, 31.38), and continuous PTSS (unstandardized B = 0.21, 95% CI 0.07, 4.19; p = 0.043). Less reduction in CRP risk categories predicted both PTSS caseness (OR 4.14, 95% CI 1.89, 9.06) and continuous PTSS (B = 1.80, 95% CI 1.09, 2.51; p < 0.001).

CONCLUSIONS:

Persistently heightened inflammation seems to be predictive for the development of PTSS three months after ACS, so interventions to lower inflammation might be warranted.

KEYWORDS:

Cardiovascular disease; Inflammation; Psychobiology; Risk factor; Trauma stress

[Indexed for MEDLINE]

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