Objective: Growing longitudinal research has demonstrated that posttraumatic stress disorder (PTSD) precedes and predicts the onset of cardiovascular disease (CVD), and a number of physiological (e.g., dysregulation of the hypothalamic-pituitary-adrenal axis and autonomic nervous system, chronic systemic inflammation) and behavioral (e.g., physical inactivity, smoking, poor diet) factors might underlie this association. In this narrative review, we focus on sleep as a modifiable risk factor linking PTSD with CVD. Method: We summarize the evidence for sleep disturbance after trauma exposure and the potential cardiotoxic effects of poor sleep, with an emphasis on mechanisms. In addition, we review the literature that has examined sleep in the context of the PTSD-CVD risk relation. Results: Although sleep disturbance is a hallmark symptom of PTSD and a well-established risk factor for the development of CVD, the role of sleep in the association between PTSD and CVD has been largely unexamined in the extant literature. However, such work has the potential to improve our understanding of mechanisms of risk and inform intervention efforts to offset elevated CVD risk after trauma. Conclusions: We outline several recommendations for future research and behavioral medicine models in order to help define and address the role of sleep behavior in the development of CVD among trauma-exposed individuals with PTSD.

Background. Posttraumatic stress disorder (PTSD) symptoms can develop following acute, life-threatening medical events. This study explores a potential biomarker of PTSD risk that is novel to a medical trauma population: a noninvasive, mobile skin conductance (SC) measurement. Methods. Participants ( n = 64 ) were enrolled inhospital following a stroke or transient ischemic attack (TIA). Mobile measurement of SC reactivity to recalling the stroke/TIA traumatic event was conducted at hospital bedside in the days following the stroke/TIA. PTSD symptoms that developed in response to the stroke/TIA were measured at 1-month follow-up. We tested the association between SC reactivity and total 1-month PTSD symptoms, as well as PTSD symptom dimensions of fear and dysphoria. Results. In unadjusted analyses, there were significant positive associations between inhospital SC reactivity to recalling the stroke/TIA traumatic event and higher-order fear-related symptoms ( r = .30 , p = .016 ), as well as lower-order fear-related symptoms of anxious arousal ( r = .27 , p = .035 ) and avoidance ( r = .25 , p = .043 ) at 1 month. Associations between SC reactivity and the fear, anxious arousal, and avoidance symptom dimensions remained significant in multivariable regression models that adjusted for relevant covariates including age, gender, stroke severity, medical comorbidity, and psychosocial factors. Although there was a positive association observed between SC reactivity to recalling the stroke/TIA event and total PTSD symptom severity at 1-month follow-up, it did not reach the level of statistical significance ( r = .23 , p = .070 ). Further, no significant association was detected for dysphoria-related symptoms ( r = .11 , p = .393 ). Conclusions. This is the first study to test the prospective association of SC reactivity with PTSD symptom development following a medical trauma. The findings indicate that mobile measures of SC reactivity may be useful for inhospital identification of individuals at risk for fear-related PTSD symptom development following a medical event and highlight the potential mechanisms involved in the development of these symptoms following a medical event.

Objective Although several risk factors for stroke-induced posttraumatic stress disorder (PTSD) have been identified, objective risk measures that can be detected in the acute aftermath of these events are needed. This study is the first to collect an objective measure of psychophysiological arousal—skin conductance (SC) reactivity to a trauma interview—in patients after stroke or transient ischemic attack (TIA) and investigate correlates of SC reactivity. Methods Mobile SC measurement during a resting baseline and standardized trauma interview was performed in-hospital in 98 individuals following stroke/TIA. We examined associations between several stroke-induced PTSD risk factors (sociodemographic, psychosocial, and medical characteristics) and SC reactivity to a trauma interview involving a free-response recalling of the stroke/TIA event. Results Of the sociodemographic, psychosocial, medical characteristics examined as correlates to SC reactivity to recalling the stroke/TIA event, 2 factors reflecting aspects of prior and in-hospital experience were significantly associated with this indicator of sympathetic nervous system activation. A greater cumulative trauma burden was significantly associated with greater SC reactivity ( r = .23, P = .04). Additionally, individuals administered benzodiazepines in-hospital had significantly greater SC reactivity to recalling the stroke/TIA event ( M = 1.51, SD = 1.52) than those who were not ( M = 0.76, SD = 1.16; P = .01). Greater cumulative trauma burden remained significantly associated with greater SC reactivity when adjusting for age and in-hospital benzodiazepine administration ( β=0.22, P = .04). Conclusion This study demonstrated that SC reactivity was related to both behavioral and psychological risk factors for PTSD after a stroke/TIA event. Additionally, we demonstrated the feasibility of a low-cost, mobile measurement of SC that can be conducted in-hospital in a novel patient population: individuals with a medical trauma. With this measure, we were able to identify those individuals with the greatest trauma-related sympathetic nervous system reactivity in the days following a medical trauma. Future research is needed to determine whether SC reactivity may be leveraged in the development of brief, noninvasive screening measures for enhancing PTSD risk prediction.