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Objective: A hypercoagulable state before overt thrombosis resulting from an imbalance between the coagulation and fibrinolysis systems is related to cardiovascular disease progression and acute coronary syndromes. Psychological stressors and depressive and anxiety disorders also are associated with coronary artery disease. This review explores whether changes in blood coagulation, anticoagulant, and fibrinolytic activity may constitute psychobiological pathways that link psychological factors with coronary syndromes.Methods: Literature on coagulation, anticoagulation, and fibrinolysis measures in conjunction with psychological factors (mental stress, psychosocial strain, and psychiatric disorders) was identified by MEDLINE search back to 1966 and through checking the bibliographies of these sources. Sixty-eight articles were critically reviewed.Results: In healthy subjects, acute mental stress simultaneously activates coagulation (ie, fibrinogen or von Willebrand factor) and fibrinolysis (ie, tissue-type plasminogen activator) within a physiological range. In patients with atherosclerosis and impaired endothelial anticoagulant function, however, procoagulant responses to acute stressors may outweigh anticoagulant mechanisms and thereby promote a hypercoagulable state. Chronic psychosocial stressors (job strain or low socioeconomic status) are related to a hypercoagulable state reflected by increased procoagulant molecules (ie, fibrinogen or coagulation factor VII) and by reduced fibrinolytic capacity. There is also some evidence that points to hypercoagulability in depression.Conclusions: Different categories of psychological measures to varying extent are associated with characteristic patterns of coagulation and fibrinolysis activity. Associations between psychological factors and several coagulation and fibrinolysis variables related to atherosclerosis provide a plausible biobehavioral link to coronary artery disease. [ABSTRACT FROM AUTHOR]

METHODS: We investigated the possibility of carotid baroreflex dysfunction as the cause of cerebral insufficiency in head and neck cancer patients treated with neck radiotherapy. Three patients cured with radiation therapy were evaluated for light-headedness and syncope. Orthostatic blood pressure, heart rate responses to esmolol and atropine, and baroreceptor sensitivity to amyl nitrite and phenylephrine were measured. The results were compared with measurements in six normal control subjects. RESULTS: All three patients had intact sympathetic and parasympathetic cardiac innervation. Nevertheless, their heart rate responses to amyl-nitrite-induced hypotension and phenylephrine hypertension were only one-third normal (P = 0.013), indicating poor baroreceptor function. Upon standing, diastolic pressure of control participants increased but that of the three patients decreased by 3 mmHg. After inhalation of amyl nitrite their systolic and diastolic blood pressures decreased by 70+/-9 and 28+/-2 mmHg, much more than the control participants' decrease of 33+/-5 and 17+/-3 mmHg (P = 0.006, P = 0.02). CONCLUSION: The baroreflex is the most important mechanism for short-term blood pressure homeostasis. Patients with transient light-headedness or syncope after radiotherapy to the neck may have baroreceptor damage. This defect is unlikely to be apparent on routine cardiovascular testing. However, testing with a rapidly acting hypotensive stimulus can reveal gross deficits in the regulation of heart rate and blood pressure.

In this study, we tested the validity of a new method designed to estimate baroreflex control of heart rate from spontaneous changes in systolic pressure and pulse interval. This method was compared with a conventional method of assessing baroreflex control through measuring reflex adjustments in pulse interval associated with pharmacological manipulations of blood pressure. The estimates of baroreflex control derived from the two methods were significantly correlated; however, only the estimate derived using pharmacological changes in pressure detected significant impairment of baroreflex control in patients with damage to baroafferents produced by radiation for oropharyngeal cancer. Analysis of spontaneous changes in pressure and pulse interval therefore provide a meaningful estimate of baroreflex control of heart rate that is, however, less sensitive than estimates obtained using pharmacological manipulations in pressure.