Common pathways and communication between the brain and heart: connecting post-traumatic stress disorder and heart failure

Abstract

Psychiatric illnesses and cardiovascular disease (CVD) contribute to significant overall morbidity, mortality, and health care costs, and are predicted to reach epidemic proportions with the aging population. Within the Veterans Administration (VA) health care system, psychiatric illnesses such as post-traumatic stress disorder (PTSD) and CVD such as heart failure (HF), are leading causes of hospital admissions, prolonged hospital stays, and resource utilization. Numerous studies have demonstrated associations between PTSD symptoms and CVD endpoints, particularly in the Veteran population. Not only does PTSD increase the risk of HF, but this relationship is bi-directional. Accordingly, a VA-sponsored conference entitled "Cardiovascular Comorbidities in PTSD: The Brain-Heart Consortium" was convened to explore potential relationships and common biological pathways between PTSD and HF. The conference was framed around the hypothesis that specific common systems are dysregulated in both PTSD and HF, resulting in a synergistic acceleration and amplification of both disease processes. The conference was not intended to identify all independent pathways that give rise to PTSD and HF, but rather identify shared systems, pathways, and biological mediators that would be modifiable in both disease processes. The results from this conference identified specific endocrine, autonomic, immune, structural, genetic, and physiological changes that may contribute to shared PTSD-CVD pathophysiology and could represent unique opportunities to develop therapies for both PTSD and HF. Some recommendations from the group for future research opportunities are provided.

Keywords: Post-traumatic stress disorder; Veterans Affairs; cardiovascular disease; heart failure; inflammation; orexin/hypocretin.

Figure 1:. Mediators and modulators of the co-morbidity between PTSD and heart failure.

Diagram shows that stress, such as experiences during combat, influences multiple systems in the brain and heart that can serve to induce PTSD as well as cardiovascular diseases. Mounting evidence suggests that the co-morbidities between PTSD and heart failure might be due to similar autonomic nervous system dysregulation, similar genetic polymorphisms, and/or common changes in cell signaling, communication and remodeling, plus immune dysregulation. Sleep dysregulation, gender, aging and metabolic disorders can all modify the severity and progression of PTSD and heart failure symptoms, but it is yet unknown how these modifiers contribute to the comorbidity between PTSD and heard failure.