Key result
Shared autonomic, inflammatory, and neuroendocrine pathways link PTSD and HF, highlighting shared therapeutic targets.
Why the study?
PTSD and heart failure are leading causes of hospitalization with a bidirectional relationship, prompting a need to explore shared biological pathways and modifiable mediators between them.
A VA-sponsored conference identified shared biological pathways between PTSD and heart failure, highlighting opportunities for future research and therapeutic development.
Shared PTSD-HF pathways remain hypothesis-generating; prospective trials required before considering joint therapeutic targets.
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.
No takes yet. Share an insight, caveat, or question.
Wilson et al. (2019) conducted a review in Post-traumatic stress disorder (PTSD) and Heart Failure (HF). Post-traumatic stress disorder (PTSD) was evaluated. Post-traumatic stress disorder and heart failure share common biological pathways, including dysregulation of the autonomic nervous system, inflammation, and neuroendocrine systems, presenting opportunities for joint therapeutic targets.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: