Semin Thromb Hemost 2013; 39(08): 902-912
DOI: 10.1055/s-0033-1357487
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Stress and Hemostasis: An Update

Anthony W. Austin
1   Montreal Behavioural Medicine Centre, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada
2   Department of Exercise Science, Concordia University, Montréal, Quebec, Canada
3   Research Centre, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada
,
Thomas Wissmann
4   Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland
,
Roland von Kanel
4   Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland
5   Department of Clinical Research, University of Bern, Bern, Switzerland
6   Psychocardiology Unit, Cardiovascular Prevention and Rehabilitation, Swiss Cardiovascular Center, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland
› Author Affiliations
Further Information

Publication History

Publication Date:
10 October 2013 (online)

Abstract

Numerous naturalistic, experimental, and mechanistic studies strongly support the notion that—as part of fight-or-flight response—hemostatic responses to acute psychosocial stress result in net hypercoagulability, which would protect a healthy organism from bleeding in case of injury. Sociodemographic factors, mental states, and comorbidities are important modulators of the acute prothrombotic stress response. In patients with atherosclerosis, exaggerated and prolonged stress-hypercoagulability might accelerate coronary thrombus growth following plaque rupture. Against a background risk from acquired prothrombotic conditions and inherited thrombophilia, acute stress also might trigger venous thromboembolic events. Chronic stressors such as job strain, dementia caregiving, and posttraumatic stress disorder as well as psychological distress from depressive and anxiety symptoms elicit a chronic low-grade hypercoagulable state that is no longer viewed as physiological but might impair vascular health. Through activation of the sympathetic nervous system, higher order cognitive processes and corticolimbic brain areas shape the acute prothrombotic stress response. Hypothalamic–pituitary–adrenal axis and autonomic dysfunction, including vagal withdrawal, are important regulators of hemostatic activity with longer lasting stress. Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response. Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed. Restoring normal hemostatic function with biobehavioral interventions bears the potential to ultimately decrease the risk of thrombotic diseases.

 
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