A new cohort study investigates the relationship between post-traumatic stress disorder (PTSD) and endothelial dysfunction, a precursor to cardiovascular disease (CVD). Conducted by researchers at the University of California, Los Angeles, this study aims to understand how trauma exposure and specific PTSD symptom dimensions relate to cardiovascular health risks.
The study highlights a pressing public health concern: both trauma exposure and PTSD are linked to a heightened risk of CVD, the leading cause of death in the United States. Endothelial dysfunction can be identified early and is modifiable, making it a prime target for interventions aimed at reducing cardiovascular risk.
The research features a sample of 160 trauma-exposed adults—80 diagnosed with PTSD and 80 matched controls without current psychiatric disorders. Participants will undergo a series of assessments, including flow-mediated vasodilation (FMD), which measures endothelial function, and tests to quantify circulating levels of endothelial cell-derived microparticles (EMPs), indicators of endothelial injury.
Previous studies primarily focused on male veterans or police officers, but this research includes a diverse group of men and women exposed to various traumatic events. The goal is to determine how PTSD and its dimensions, particularly fear and dysphoria, affect endothelial dysfunction over time.
The study employs a cohort design, collecting data at baseline and following up two years later to assess changes in symptoms and vascular health. This longitudinal approach will allow researchers to examine the progression of endothelial dysfunction in relation to PTSD symptom severity.
Existing literature suggests that trauma exposure correlates with decreased endothelial function. For every 1% decline in FMD, the risk of developing CVD increases by 9-13%. Thus, understanding how PTSD symptoms influence endothelial health can inform future preventative strategies.
Participants will be assessed using a fear conditioning paradigm to measure psychophysiological responses associated with PTSD. This includes evaluations of autonomic balance, inflammation, and oxidative stress as potential mechanisms linking PTSD symptoms to endothelial dysfunction.
The findings from this study could lead to more targeted interventions for individuals suffering from PTSD, aiming to mitigate their risk of cardiovascular disease. By identifying specific PTSD symptom dimensions that impact vascular health, healthcare providers can better monitor and support trauma-exposed individuals.
This research contributes to the growing body of evidence underscoring the links between mental health and physical health, particularly the physiological effects of trauma and PTSD on cardiovascular systems. As trauma is prevalent—affecting 50-90% of individuals at some point in their lives—understanding its long-term health effects is vital.
The study is registered under the clinical trial number NCT03778307 and is set to continue through 2023, with results expected to be published in peer-reviewed journals and shared with community partners. The research adheres to ethical standards outlined in the Helsinki Declaration and has received approval from the University of California, Los Angeles Institutional Review Board.