, 62, is one psychoanalyst willing to declare that Richard Nixon's phlebitis is psychosomatic. The man has been under extraordinary pressure for more than a year, Dr. Silverman says. Mr. Nixon seems to keep his emotions under such control that we might have expected physical instead of emotional breakdown.Time Magazine, September 30, 1974, p. 65. This introductory "case vignette" raises the question of whether intense emotional stress, such as experienced by the United States President Nixon in the wake of the Watergate scandal, is capable of causing thrombosisassociated diseases and, if so, by which mechanisms. Thus, the aim of this review is to provide an update on the sizeable literature on stress-related changes in the Keywords ► blood coagulation ► fibrinolysis ► platelets ► psychological stress ► risk factor AbstractNumerous 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. hemostatic system (i.e., coagulation, fibrinolysis, and platelets) and their potential role in thrombosis. As a prerequisite for the notion that stress-associated hypercoagulability contributes to thrombotic events, 1 abundant epidemiological and experimental data exist supporting the role of enhanced coagulation, impaired fibrinolysis, and hyperactive platelets in the development of atherogenesis, atherothrombosis, and acute coronary...

Traditional methods of adjusting for stress-hemoconcentration effects (e.g., calculated plasma volume or hematocrit level corrections) may not be appropriate when examining stress-induced changes in hemostasis. The effects of acute stress on hemostasis should be examined in conjunction with hemoconcentration.

Results emphasize the importance of considering hydration status and blood pressure when interpreting cognitive performance in older adults.

The observed changes in coagulation are likely in part a consequence of stress and hemoconcentration, but the DCC seems to be an inappropriate hemoconcentration correction technique of time-dependent assays. The saline reconstitution technique may be more biologically relevant when examining stress-hemoconcentration effects on coagulation.