There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.

This systematic review examines the effect of diverse psychosocial stressors on polysomnographic measures of sleep. Sixty-three articles were located and categorized in terms of the types of stressors imposed. Experimental stress resulted in fairly consistent changes: decreases in slow wave sleep, REM sleep, and sleep efficiency (SE), as well as increases in awakenings. Data were limited in terms of response to non-experimental stressors, except for the case of post-traumatic stress disorder (PTSD) on sleep, where a number of reports suggest that PTSD patients have increased awakenings and decreased SE. Future research needs to define stress more precisely in terms of duration and severity and to measure its impacts on sleep in populations that differ in terms of age, comorbid illness, gender, and so forth. Without such fine-grained analyses, it is difficult to draw definitive conclusions about this important area.Sleep researchers traditionally have focused on primary sleep disorders such as sleep apnea, narcolepsy, or periodic limb movement disorder; but common knowledge has it that the stresses of daily life can perturb even healthy sleep. As Mason (1968) described, psychological stressors are potent stimuli for physiological stress responses. Most studies on psychosocial stress and its physiological effects on sleep are based solely on subjective reports. However, these subjective reports of sleep are not sufficient to evaluate physiological sleep changes as measured by polysomnography (PSG; Akerstedt, Hume, Minors, & Waterhouse, 1994;Schneider-Helmert & Kumar, 1995). What really happens in sleep physiology after exposure to stressors? Although the gold standard of measurement of sleep is PSG, there are relatively little data concerning the effects of ordinary or severe stress on polysomnographically examined sleep. This article systematically reviews the diverse literature in this area.Stress is notorious for being difficult to define. It encompasses all kinds of stimuli of varying amounts of aversiveness and duration (Dimsdale, Irwin, Keefe, & Stein, 2005). Kecklund and Akerstedt (2004b) grouped stressors conceptionally into physical versus psychological or social, acute versus chronic, and high intensity versus low intensity.Copyright © Lawrence Erlbaum Associates, Inc. Correspondence should be addressed to Joel E. Dimsdale, University of California, San Diego, 9500 Gilman D., La Jolla, CA 92093-0804. jdimsdale@ucsd.edu. NIH Public Access Author ManuscriptBehav Sleep Med. Author manuscript; available in PMC 2014 December 15. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptAlthough there are numerous animal models of social stress, it is still challenging to generalize psychosocial stress responses in animals to those in humans. This review focuses on psychosocial stressors; other types of stressors such as environmental manipulations (e.g., temperature), exercise, or intentionally imposed sleep disruption are not covered in this article.It is possible that different types...

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.

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Overactivity of the sympathetic nervous system (SNS) has been related to increased cardiovascular morbidity. Historical reports suggest hastening of blood coagulation following intravenous administration of epinephrine. Given the important role of the hemostatic system in atherosclerosis and thrombosis, it is surprising that short-term adrenergic effects on blood coagulation, fibrinolysis and platelet activity have not been scrutinized closely. To elucidate such effects in vivo, this paper reviews human studies in which alpha- and beta-sympathomimetic agents had been infused. The literature suggests a dose-dependent stimulation of factor VIII clotting activity, von Willebrand factor antigen, tissue-type plasminogen activator, and platelets within a 15- to 40-min infusion of epinephrine. Precise mechanisms underlying hemostatic changes with sympathetic activation remain to some extent speculative. However, there is evidence from adrenoreceptor blockade studies that coagulation and fibrinolysis molecules are released into circulation by stimulation of vascular endothelial beta-adrenoreceptors (most likely beta2-receptors). Combined alpha2- and beta2-adrenoreceptor-related mechanism(s) are responsible for platelet activation. Short-term activation of the SNS effects regular hemostatic activity. While in healthy individuals the hemostatic balance between coagulation and fibrinolysis may be preserved, catecholamine surge may trigger a hypercoagulable state and enhance the odds of overt thrombosis in patients with atherosclerotic disease.