Background and Purpose— In older populations, transient ischemic attack (TIA) and ischemic stroke have been linked to psychological factors, including posttraumatic stress disorder (PTSD). Whether PTSD also increases risk for early incident stroke in young adults is unknown. Methods— We prospectively assessed the incidence of TIA and ischemic stroke in a cohort of 987 855 young and middle-aged Veterans (mean age of 30.29±9.19 years; 87.8% men, 64.4% white) who first accessed care through the Veterans Health Administration from October 2001 to November 2014 and were free of TIA and ischemic stroke at baseline. For each outcome, time-varying multivariate Cox models were constructed to examine the effect of PTSD on incident stroke. We also assessed for effect modification by sex. Additional sensitivity analyses controlled for healthcare utilization. Results— Over a 13-year period, TIA and ischemic stroke were diagnosed in 766 and 1877 patients, respectively. PTSD was diagnosed in 28.6% of the sample during follow-up. In unadjusted analyses, PTSD was significantly associated with new-onset TIA (hazard ratio [HR], 2.02; 95% CI, 1.62–2.52) and ischemic stroke (HR, 1.62; 95% CI, 1.47–1.79). In fully adjusted models, the association between PTSD and incident TIA (HR, 1.61; 95% CI, 1.27–2.04) and ischemic stroke (HR, 1.36; 95% CI, 1.22–1.52) remained significant. The effect of PTSD on ischemic stroke risk was stronger in men than in women (HR, 0.63; 95% CI, 0.47–0.86; P =0.003), but no effect of sex was found for TIA. Conclusions— PTSD is associated with a significant increase in risk of early incident TIA and ischemic stroke independent of established stroke risk factors, coexisting psychiatric disorders, and healthcare utilization. Sex moderated the relationship for adults with ischemic stroke but not TIA. These findings suggest that psychological factors, including PTSD, may be important targets for future age-specific prevention strategies for young adults.
Background and Purpose: Antidepressants are commonly prescribed for posttraumatic stress disorder (PTSD) and may increase the risk of bleeding, including hemorrhagic stroke. Methods: We prospectively examined independent effects of PTSD, selective serotonin and norepinephrine reuptake inhibitors (SSRI and SNRI) on the risk of incident hemorrhagic stroke in a nationwide sample of 1.1 million young and middle-aged veterans. Time-varying multivariate Cox models were used to examine hemorrhagic stroke risk by PTSD status and use of SSRI or SNRI while adjusting for demographics, lifestyle factors, stroke, and psychiatric comorbidities. Sensitivity analyses controlled for health care utilization. Results: During 13 years of follow-up (2.14 years on average), 507 patients (12% women) suffered a hemorrhagic stroke. The overall incidence rate was 1.70 events per 10 000-person years. In unadjusted models, PTSD was associated with an 82% greater risk of new-onset hemorrhagic stroke (hazard ratio [HR], 1.82 [95% CI, 1.48–2.24]), SSRI use was associated with a >2-fold risk (HR, 2.02 [95% CI, 1.66–2.57]), and SNRI use was associated with a 52% greater risk (HR, 1.52 [95% CI, 1.08–2.16]). In fully adjusted models, effects of PTSD and SNRI were attenuated (adjusted HR, 1.03 [95% CI, 0.81–1.34]; adjusted HR, 1.19 [95% CI, 0.83–1.71]), but SSRI use remained associated with a 45% greater risk of hemorrhagic stroke (adjusted HR, 1.45 [95% CI, 1.13–1.85]). Hypertension, drug abuse, and alcohol abuse were also associated with increased stroke risk. Nonobesity and being non-Hispanic were protective factors. In sensitivity analyses, health care utilization was a small but significant predictor of stroke. Conclusions: In the largest known investigation of PTSD and antidepressant-associated risk for hemorrhagic stroke in young adults, use of SSRIs, but neither PTSD nor SNRIs were independently associated with incident stroke. SNRIs may be preferable for treating PTSD and comorbid conditions, although pursuing other modifiable risk factors and non-pharmacological treatments for PTSD also remains essential.
Sexual assault is associated with a number of health risk behaviors in women. It has been hypothesized that these risk behaviors, such as hazardous drinking, may represent women's attempts to cope with psychological distress, such as symptoms of depression and anxiety. However, extant research has failed to evaluate these relationships among ethnic minority samples or identify the mechanisms responsible for this association. The current study examined sexual assault history and two health risk behaviors (hazardous drinking and engaging in sexual behavior to regulate negative affect) in a diverse sample of 1,620 college women. Depression and anxiety were examined as mediators of the relationship between sexual assault and health risk behaviors. There was evidence of moderated mediation, such that for European American women, but not for ethnic minority women, both forms of psychological distress were significant mediators of the sexual assault/hazardous drinking relationship. In contrast, among all ethnic groups, the relationship between sexual assault and both forms of psychological distress was mediated by the use of sexual behavior as an affect regulation strategy. Results support a need to evaluate the assault experiences of ethnically diverse women, as well as the impact of the assault on their postassault experiences including health risk behaviors and psychological adjustment. Additionally, results suggest that practitioners should carefully assess health risk behaviors among victims of sexual assault and be aware that there may be differences in the risk factors and motives for these behaviors among women of various ethnic backgrounds.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.