期刊
THROMBOSIS RESEARCH
卷 135, 期 -, 页码 S52-S55出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0049-3848(15)50444-1
关键词
Blood coagulation; Cardiovascular disease; Fibrinolysis; Psychological stress; Risk factor; Thrombosis
资金
- Swiss National Science Foundation [81BE-56155, 3268277, PP00P1_128565/1]
- National Institutes of Health [MO1 RR-00827, HL-57265, AG-13332, HL-36005, HL-44915]
- National Institute on Aging [AG-15301, AG-23989]
- Swiss Federal Institute of Technology Zurich
- University of Bern, Switzerland
- University of Zurich, Switzerland
- Novartis Foundation Switzerland
- Swiss Cocoa and Chocolate Foundation
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-orflight 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. (C) 2015 Elsevier Ltd. All rights reserved.
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