title: Acute mental stress and hemostasis: When physiology becomes vascular harm.
abstract: Stress-induced activation of the sympathoadrenal medullary system activates both the coagulation and fibrinolysis system resulting in net hypercoagulability. The evolutionary interpretation of this physiology is that stress-hypercoagulability protects a healthy organism from excess bleeding should injury occur in fight-or-flight situations. In turn, acute mental stress, negative emotions and psychological trauma also are triggering factors of atherothrombotic events and possibly of venous thromboembolism. Individuals with pre-existent atherosclerosis and impaired endothelial anticoagulant function are the most vulnerable to experience onset of acute coronary events within two hours of intense emotions. A range of sociodemographic and psychosocial factors (e.g., chronic stress and negative affect) might critically intensify and prolong stress-induced hypercoagulability. In contrast, several pharmacological compounds, dietary flavanoids, and positive affect mitigate the acute prothrombotic stress response. Studies are needed to investigate whether attenuation of stress-hypercoagulability through medications and biobehavioral interventions reduce the risk of thrombotic incidents in at-risk populations.
authors.affiliation: Department of Neurology, Inselspital, Bern University Hospital, and University of Bern, Switzerland; Department of Clinical Research, University of Bern, Switzerland; Department of Psychosomatic Medicine, Clinic Barmelweid, Barmelweid, Switzerland. Electronic address: roland.vonkaenel@barmelweid.ch.
authors.forename: Roland
authors.initials: R
authors.lastname: von Känel
mesh_terms: D000208:Acute Disease; D006487:Hemostasis; D006801:Humans; D008955:Models, Cardiovascular; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology*; D013927:Thrombosis / Q000209:etiology* / Q000503:physiopathology*
keywords: Blood coagulation; Cardiovascular disease; Fibrinolysis; Psychological stress; Risk factor; Thrombosis