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Author Notes:

Dr. Viola Vaccarino, MD, PhD, Emory University, Department of Epidemiology, Rollins School of Public Health, 1518 Clifton Rd NE, Room 3011, Atlanta, GA 30322. Phone: 404-727-8710; Fax: 404-727-8737; viola.vaccarino@emory.edu

The authors report no biomedical financial interests or potential conflicts of interest.

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Research Funding:

This work was supported by the NIH, through the following grants: R01 HL109413, R01HL109413-02S1, R01 HL125246, R01 HL136205, R01 HL088726, P01 HL101398, KL2TR000455, K24HL077506, K24 MH076955, K23HL127251, and THL130025A.

This work was supported by the e National Institutes of Health Grant Nos. P01HL101398, P20HL113451, P01HL086773-06A1, R56HL126558, R01HL109413, R01HL109413-02S1, R01HL125246, UL1TR000454, KL2TR000455, K24HL077506, K24 MH076955, K23HL127251, and THL130025A.

Keywords:

  • PTSD
  • mental stress
  • myocardial infarction
  • interleukin-6
  • high-sensitivity C reactive protein
  • Matrix metallopeptidase 9
  • Monocyte chemoattractant protein-1

Posttraumatic Stress Disorder is Associated with Enhanced Interleukin-6 Response to Mental Stress in Subjects with a Recent Myocardial Infarction

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Journal Title:

BRAIN BEHAVIOR AND IMMUNITY

Volume:

Volume 75

Publisher:

, Pages 26-33

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Background: Posttraumatic Stress Disorder (PTSD) is prevalent among patients who survived an acute coronary syndrome, and is associated with adverse outcomes, but the mechanisms underlying these associations are unclear. Individuals with PTSD have enhanced sensitivity of the noradrenergic system to stress which may lead to immune activation. We hypothesized that survivors of a myocardial infarction (MI) who have PTSD would show an enhanced inflammatory response to acute psychological stress compared to those without PTSD. Methods: Individuals with a verified history of MI within 8 months and a clinical diagnosis of current PTSD underwent a mental stress speech task. Inflammatory biomarkers including interleukin-6 (IL-6), high-sensitivity C reactive protein (HsCRP), matrix metallopeptidase 9 (MMP-9), intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and monocyte chemoattractant protein (MCP)-1 were measured at rest and 90 min after mental stress. Results: Among 271 patients in the study (mean age 51 ± 7 years, 50% female, 60% African-American), the prevalence of PTSD was 12%. Mental stress resulted in a significant increase in IL-6, but the increase was more marked in patients with PTSD (126% increase) than those without (63% increase) (p=0.001). MCP-1 showed a modest increase with stress which was similar in patients with PTSD (9% increase) and without PTSD (6% increase) (p=0.35). CRP did not increase with stress in either group. Conclusion: MI patients with current PTSD exhibit enhanced IL-6 response to psychosocial stress, suggesting a mechanistic link between PTSD and adverse cardiovascular outcomes as well as other diseases associated with inflammation.

Copyright information:

© 2018 Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (https://creativecommons.org/licenses/by-nc-nd/4.0/).
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