Psychological and biological mechanisms linking trauma with cardiovascular disease risk

Abstract

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.

Fig. 1. Conceptual model of key psychological and biological mechanisms linking trauma exposure with incident cardiovascular disease (CVD).

Experiences of trauma and severe stress precede manifestations of posttraumatic psychopathology, such as posttraumatic stress disorder (PTSD) and depression. Subsequent dysregulation of biological stress response systems, including the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic-adrenal-medullary (SAM) system, can contribute to further dysregulation in several interconnected biological systems, potentially leading to immune dysregulation and elevated inflammation, oxidative stress, mitochondrial dysfunction, and dysregulation of the renin-angiotensin system (RAS). Not only can these biological processes further influence one another (as indicated by the recursive arrows), but they can also contribute to accelerated biological aging. Together, these biological alterations can lead to the accumulation of intermediary cardiovascular risk factors, such as hypertension, endothelial dysfunction, and atherosclerosis, which—in turn—increase risk of developing CVD. Furthermore, these psychological and biological processes may unfold after trauma within a milieu of shared genetic risk.