The following are key points to remember from this Special Communication on posttraumatic stress disorder (PTSD) and cardiovascular disease (CVD):

1. While not often considered a major CVD risk factor, PTSD is much more common in this era of the wars in Iraq and Afghanistan that have lasted a generation, and increase in gun violence, and racial tension.
2. PTSD is characterized by a persistent maladaptive reaction after exposure to severe psychological trauma. Traumatic events that may precipitate PTSD include violent personal assaults, natural and human-made disasters, and exposure to military combat or warfare.
3. It is not yet considered an independent risk factor, but like the metabolic syndrome, PTSD is associated with major risk factors for CVD including hypertension, dyslipidemia, and diabetes, and outcomes including myocardial infarction and heart failure. In clinical practice, it is unclear whether these associations are causal or confounded. In a cohort study, PTSD was associated with a 27% increase in incident CVD events or cardiac mortality after adjusting for depression and demographic, clinical, and psychosocial factors with similar magnitude in women and men, findings that were confirmed in a 2018 meta-analysis.
4. Pathophysiology of PTSD as a potential CVD risk factor is not well understood. At the level of neural circuits, preclinical and human studies support the concept of PTSD as a disorder of altered emotional memory formation and/or extinction and dysregulation of the response to environmental threat and stress. Brain imaging data in PTSD demonstrates changes in regions involved in emotion processing and cognition which correlate with altered behavioral manifestations including increased attentional bias to threat and exaggerated physiological, emotional, and behavioral responses to threat cues.
5. Abnormal functioning of the autonomic nervous system and inflammatory-immune response may be key pathophysiological links between PTSD and CVD. Altered functions of specific brain circuits have been linked to increased CVD morbidity and mortality with changes in catecholamines, sympathetic-parasympathetic balance, sleep, and inflammatory signaling each being hypothesized mediators.
6. The authors described the need for animal models and human tissue biobanks to help elucidate the potential causal connection of PTSD-induced brain changes and/or inflammation with CVD pathophysiology. Emerging large-scale genome-wide association studies of PTSD will provide an opportunity to conduct Mendelian randomization studies that test hypotheses regarding the presence, magnitude, and direction of causal associations between PTSD and CVD outcomes.
7. Large-scale, well-designed prospective studies, capturing diverse and high-risk populations, are warranted that include uniform phenotyping of PTSD as well as broad assessment of biological and behavioral risk factors and CVD outcomes.

Clinical Topics: Diabetes and Cardiometabolic Disease, Dyslipidemia, Heart Failure and Cardiomyopathies, Prevention, Acute Heart Failure, Hypertension

Keywords: Catecholamines, Cognition Disorders, Depression, Diabetes Mellitus, Disasters, Dyslipidemias, Emotions, Heart Failure, Hypertension, Inflammation, Metabolic Syndrome, Military Personnel, Neuroimaging, Primary Prevention, Risk Factors, Sleep Wake Disorders, Stress Disorders, Post-Traumatic, Trauma, Nervous System

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