Bruno B Lima1, Muhammad Hammadah2, Kobina Wilmot2, Brad D Pearce3, Amit Shah4, Oleksiy Levantsevych2, Belal Kaseer2, Malik Obideen2, Mohamad Mazen Gafeer2, Jeong Hwan Kim2, Samaah Sullivan3, Tené T Lewis3, Lei Weng5, Lisa Elon5, Lian Li3, J Douglas Bremner6, Paolo Raggi7, Arshed Quyyumi2, Viola Vaccarino8. 1. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States; Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States. 2. Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States. 3. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States. 4. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States; Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States; Atlanta VA Medical Center, Decatur, GA, United States. 5. Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, United States. 6. Atlanta VA Medical Center, Decatur, GA, United States; Departments of Psychiatry and Behavioral Sciences and Radiology, Emory University School of Medicine, United States. 7. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States; Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada. 8. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States; Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States. Electronic address: viola.vaccarino@emory.edu.
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.
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.
Authors: Muhammad Hammadah; Ayman Alkhoder; Ibhar Al Mheid; Kobina Wilmot; Nino Isakadze; Naser Abdulhadi; Danielle Chou; Malik Obideen; Wesley T O'Neal; Samaah Sullivan; Ayman Samman Tahhan; Heval Mohamed Kelli; Ronnie Ramadan; Pratik Pimple; Pratik Sandesara; Amit J Shah; Laura Ward; Yi-An Ko; Yan Sun; Irina Uphoff; Brad Pearce; Ernest V Garcia; Michael Kutner; J Douglas Bremner; Fabio Esteves; David S Sheps; Paolo Raggi; Viola Vaccarino; Arshed A Quyyumi Journal: Int J Cardiol Date: 2017-05-25 Impact factor: 4.164
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Authors: Bruno B Lima; Muhammad Hammadah; Brad D Pearce; Amit Shah; Kasra Moazzami; Jeong Hwan Kim; Samaah Sullivan; Oleksiy Levantsevych; Tené T Lewis; Lei Weng; Lisa Elon; Lian Li; Paolo Raggi; J Douglas Bremner; Arshed Quyyumi; Viola Vaccarino Journal: JAMA Netw Open Date: 2020-04-01