Background: Posttraumatic stress disorder (PTSD) is associated with interpersonal dysfunction and adverse maternal health during the perinatal period (extending from conception through one year postpartum). However, PTSD is a heterogeneous disorder, and little is known about which aspects of this disorder may be particularly deleterious to the health of new mothers. Such data may inform more personalized approaches to PTSD prevention and treatment among postpartum women. Methods: Using confirmatory factor analysis, we compared three models of PTSD symptom structure-the fourfactor dysphoria model, four-factor emotional numbing model, and five-factor dysphoric arousal model-in 1,663 postpartum women from the Community and Child Health Network (CCHN). We examined associations between PTSD symptom dimensions of the best-fitting model with four correlates relevant to maternal health and functioning-parenting stress, partner relationship stress, relationship satisfaction, and contraceptive use.Results: Though all models fit well, the five-factor dysphoric arousal model provided optimal fit. Symptom dimensions from this model-re-experiencing, avoidance, numbing, dysphoric arousal, and anxious arousal-evidenced differential associations with the maternal health indicators. Numbing symptoms were most strongly associated with indicators of poor interpersonal functioning, whereas dysphoric arousal symptoms were most strongly related to low-efficacy contraceptive use. Limitations: Our cross-sectional study assessed DSM-IV PTSD symptoms. Conclusions: PTSD symptoms among postpartum women are best-represented by five factors. Numbing symptoms (e.g., restricted affect, detachment) are most strongly associated with interpersonal difficulties, whereas dysphoric arousal symptoms (e.g., agitation, irritability) are linked with low-efficacy contraceptive use. Screening for these symptoms may help promote the health of new mothers.
Cardiovascular disease (CVD) is the leading cause of death and disability worldwide, and experiences of psychological trauma have been associated with subsequent CVD onset. Identifying key pathways connecting trauma with CVD has the potential to inform more targeted screening and intervention efforts to offset elevated cardiovascular risk. In this narrative review, we summarize the evidence for key psychological and biological mechanisms linking experiences of trauma with CVD risk. Additionally, we describe various methodologies for measuring these mechanisms in an effort to inform future research related to potential pathways. With regard to mechanisms involving posttraumatic psychopathology, the vast majority of research on psychological distress after trauma and CVD has focused on posttraumatic stress disorder (PTSD), even though posttraumatic psychopathology can manifest in other ways as well. Substantial evidence suggests that PTSD predicts the onset of a range of cardiovascular outcomes in trauma-exposed men and women, yet more research is needed to better understand posttraumatic psychopathology more comprehensively and how it may relate to CVD. Further, dysregulation of numerous biological systems may occur after trauma and in the presence of posttraumatic psychopathology; these processes of immune system dysregulation and elevated inflammation, oxidative stress, mitochondrial dysfunction, renin-angiotensin system dysregulation, and accelerated biological aging may all contribute to subsequent cardiovascular risk, although more research on these pathways in the context of traumatic stress is needed. Given that many of these mechanisms are closely intertwined, future research using a systems biology approach may prove fruitful for elucidating how processes unfold to contribute to CVD after trauma.
IntroductionBoth trauma exposure and post-traumatic stress disorder (PTSD) are associated with increased risk of cardiovascular disease (CVD), the leading cause of death in the USA. Endothelial dysfunction, a modifiable, early marker of CVD risk, may represent a physiological mechanism underlying this association. This mechanism-focused cohort study aims to investigate the relationship between PTSD (both in terms of diagnosis and underlying symptom dimensions) and endothelial dysfunction in a diverse, community-based sample of adult men and women.Methods and analysisUsing a cohort design, 160 trauma-exposed participants without a history of CVD are designated to the PTSD group (n=80) or trauma-exposed matched control group (n=80) after a baseline diagnostic interview assessment. Participants in the PTSD group have a current (past month) diagnosis of PTSD, whereas those in the control group have a history of trauma but no current or past psychiatric diagnoses. Endothelial dysfunction is assessed via flow-mediated vasodilation of the brachial artery and circulating levels of endothelial cell-derived microparticles. Two higher order symptom dimensions of PTSD—fear and dysphoria—are measured objectively with a fear conditioning paradigm and attention allocation task, respectively. Autonomic imbalance, inflammation, and oxidative stress are additionally assessed and will be examined as potential pathway variables linking PTSD and its dimensions with endothelial dysfunction. Participants are invited to return for a 2-year follow-up visit to reassess PTSD and its dimensions and endothelial dysfunction in order to investigate longitudinal associations.Ethics and disseminationThis study is conducted in compliance with the Helsinki Declaration and University of California, Los Angeles Institutional Review Board. The results of this study will be disseminated via articles in peer-reviewed journals and presentations at academic conferences and to community partners.Trial registration numberNCT03778307; pre-results.
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