Oxidative stress and impaired cardiovagal baroreflex sensitivity in young adults with post‐traumatic stress disorder

Post-traumatic stress disorder (PTSD) is associated with elevated cardiovascular disease (CVD) risk, yet the underlying physiological characterization in young adults remain unclear. This study examines whether autonomic and/or vascular dysfunction predominates as an early precursor to CVD development in young adults with PTSD and explores the potential contribution of oxidative stress (OXS). Forty-four young adults (22 PTSD, 22 controls; 19F/3M per group) free from cardiometabolic disease were evaluated for OXS, autonomic regulation and vascular function. OXS was quantified via electron paramagnetic resonance analysis of whole blood superoxide concentration. Autonomic function was assessed using an isometric handgrip exercise (exercise pressor reflex) and a Valsalva manoeuvre to determine cardiovagal baroreflex sensitivity (cBRS). Local vascular control was evaluated through rapid onset vasodilation (ROV) in response to a brief forearm contraction. Compared with controls, the PTSD group exhibited significantly higher resting systolic (P < 0.01) and mean arterial pressure (P = 0.04) and elevated superoxide levels (P < 0.01). cBRS was markedly reduced in PTSD during Phase IV of the Valsalva manoeuvre (P < 0.01), indicating impaired autonomic regulation. In contrast, vascular conductance and blood flow responses to the ROV and exercise pressor tests were preserved. These findings suggest that OXS and baroreflex dysfunction, rather than local vascular impairment, represent early detectable maladaptations potentially contributing to heightened CVD risk in young adults with PTSD. Early identification and mitigation of oxidative and autonomic imbalances may help prevent premature cardiovascular decline in this population.