Post-Traumatic Stress Disorder and Atherosclerosis: Co-Phenomena, or Cause-and-Effect?

Post-traumatic stress disorder (PTSD), a trauma- and stressor-triggered psychiatric condition affecting approximately 10 million Americans, is a major risk factor for atherosclerosis and its devastating sequelae including ischemic heart disease, stroke and hypertension. PTSD and atherosclerosis share many pathogenic mechanisms impacting the limbic system, prefrontal cortex and systemic vasculature, including hyperactivation of the sympathetic and renin-angiotensin systems, inflammation, dysregulated coagulation and altered cortisol secretion. Whether PTSD is a direct cause of atherosclerosis, or an independent co-phenomenon, is an unresolved but pivotal question.

Recent evidence supports both sequential cause-and-effect, where PTSD-instigated mechanisms provoke and/or perpetuate atherosclerosis, and parallel development of both phenomena from shared trauma-activated mechanisms. Mounting evidence also supports a bidirectional interaction, wherein the cardiovascular consequences of atherosclerosis elicit chronic psychiatric stress and, potentially, a maladaptive feedforward PTSD - atherosclerosis cycle. The specific pathobiological context may determine the prevailing relationship. Recent research has revealed multifaceted interactions among the neuroendocrine cascades mediating PTSD and atherosclerosis, and demonstrated complex associations between the two disorders. Knowledge of the PTSD - atherosclerosis relationship in the individual patient will inform efforts to optimize treatment of these complicated conditions.