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Impact of cognitive behavioural therapy on neural, inflammatory, & autonomic markers in a sample with PTSD and
Robyn Ellis1,2, Sinead Sinnott1,2, Krystel Karam3,4
1Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Abstract:
Background: Individuals with posttraumatic stress disorder (PTSD) are at heightened risk for cardiovascular disease (CVD) compared to the general population. Inflammation and autonomic dysfunction are candidate mechanisms of CVD risk in PTSD; however, these mechanisms have not been well-characterised in the PTSD-CVD link. Further, these mechanisms may operate through altered stress-related neural activity (SNA). Yet, it remains unknown if changes in PTSD are associated with changes in CVD risk mechanisms.Objective: This manuscript describes the design and procedures of a pilot randomised controlled trial to assess the impact of a first-line treatment for PTSD (Cognitive Processing Therapy; CPT) versus waitlist control on mechanisms of CVD risk. Further, this study will test the hypothesis that CPT reduces CVD risk through its effects on inflammation and autonomic function and that these changes are driven by changes in SNA.Methods: Adults with PTSD and CVD risk (N = 30) will be randomised to CPT or waitlist control. Participants complete two laboratory visits (baseline and post-treatment) that include surveys, brain and peripheral imaging via 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), and resting measures of autonomic function. Primary outcomes include arterial inflammation and heart rate variability. Secondary outcomes include leukopoiesis (bone marrow uptake), heart rate, and blood pressure. The indirect effects of PTSD treatment on changes in inflammation and autonomic function through SNA will also be examined.Conclusions: This study seeks to characterise candidate neuroimmune mechanisms of the PTSD-CVD link to identify treatment targets and develop personalised interventions to reduce CVD events in PTSD populations.Trial registration: ClinicalTrials.gov identifier: NCT06429293..
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