Stress and Hemostasis: An Update

Abstract

, 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...

Anxiety, Depression, and Adverse Clinical Outcomes in Patients With Atrial Fibrillation Starting Warfarin: Cardiovascular Research Network WAVE Study

“…Information on certain behavioral factors (eg, smoking and physical inactivity)31 that may potentially confound the relationship between anxiety and outcomes was not consistently available and, thus, could not be analyzed. An intriguing avenue of further investigation may be how anxiety‐related stress can lead to alterations in hemostasis 32, 33. Autonomic arousal in the context of anxiety may result in physiologic changes, such as an increase in blood pressure,34 that are associated with the risk of both ischemic stroke and intracranial bleeding events.…”

Consumo alimentar e estresse em pacientes com síndrome coronariana aguda

“…As for the acute onset of cardiac events, psychological stress causes a series of physiological responses that can trigger ACS in patients with CAD. Acute mental stress (through the autonomic nervous system and neuroendocrine response) leads to activation and increase in the number of platelets, development and worsening of the endothelial dysfunction, inflammatory response and pro-thrombotic phenomena, with a potential for disruption of a vulnerable plaque and precipitation of the intraluminal thrombus, resulting in AMI (26) . Among 4204 patients with a mean age of 59 years, 67% men and 67% white discharged from 24 hospitals in the United States after AMI, 38.6% reported moderate or high levels of stress in the four weeks prior to the event (27) .…”

Myocardial Infarction, Unstable Angina, and White Thrombi: Time to Move Forward?

“…Other than the preceding responses, related to earlier parts of the correspondence, we have no specific comments on the role of anxiety and depression in the pathogenesis of acute coronary syndrome. A comprehensive discussion about the interplay between stress and hemostasis has already been published within Seminars in Thrombosis and Hemostasis, 12 and we also provided recent updates on the association between cardiovascular disease and mental depression in one of our other articles. 13 It is thus substantially likely that both these conditions (anxiety and depression) may represent putative triggers, or contributing factors, of AMI, although their relationship with the nature and structure of coronary thrombi is currently lacking any reliable scientific evidence.…”