Author: Antonia V Seligowski1, Simran S Grewal2, Shady Abohashem3, Hadil Zureigat3, Iqra Qamar3, Wesam Aldosoky3, Charbel Gharios4, Erin Hanlon4, Omar Alani4, Sandeep C Bollepalli5, Antonis Armoundas6, Zahi A Fayad7, Lisa M Shin8, Michael T Osborne3, Ahmed Tawakol3
Affiliation:
1 Deparment of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
2 Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: aseligowski@mgh.harvard.edu.
3 Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
4 Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
5 Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
6 Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; Broad Institute, Massachusetts Institute of Technology, Cambridge, MA, USA.
7 BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
8 Deparment of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Department of Psychology, Tufts University, Medford, MA, USA.
Conference/Journal: Brain Behav Immun
Date published: 2024 Jan 11
Other:
Volume ID: 117 , Pages: 149-154 , Special Notes: doi: 10.1016/j.bbi.2024.01.006. , Word Count: 221
While posttraumatic stress disorder (PTSD) is known to associate with an elevated risk for major adverse cardiovascular events (MACE), few studies have examined mechanisms underlying this link. Recent studies have demonstrated that neuro-immune mechanisms, (manifested by heightened stress-associated neural activity (SNA), autonomic nervous system activity, and inflammation), link common stress syndromes to MACE. However, it is unknown if neuro-immune mechanisms similarly link PTSD to MACE. The current study aimed to test the hypothesis that upregulated neuro-immune mechanisms increase MACE risk among individuals with PTSD. This study included N = 118,827 participants from a large hospital-based biobank. Demographic, diagnostic, and medical history data collected from the biobank. SNA (n = 1,520), heart rate variability (HRV; [n = 11,463]), and high sensitivity C-reactive protein (hs-CRP; [n = 15,164]) were obtained for a subset of participants. PTSD predicted MACE after adjusting for traditional MACE risk factors (hazard ratio (HR) [95 % confidence interval (CI)] = 1.317 [1.098, 1.580], β = 0.276, p = 0.003). The PTSD-to-MACE association was mediated by SNA (CI = 0.005, 0.133, p < 0.05), HRV (CI = 0.024, 0.056, p < 0.05), and hs-CRP (CI = 0.010, 0.040, p < 0.05). This study provides evidence that neuro-immune pathways may play important roles in the mechanisms linking PTSD to MACE. Future studies are needed to determine if these markers are relevant targets for PTSD treatment and if improvements in SNA, HRV, and hs-CRP associate with reduced MACE risk in this patient population.
Keywords: Autonomic; Cardiovascular; Inflammation; Neural; PTSD.
PMID: 38218349 DOI: 10.1016/j.bbi.2024.01.006
