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A large body of empirical research shows that psychosocial risk factors (PSRFs) such as low socio-economic status, social isolation, stress, type-D personality, depression and anxiety increase the risk of incident coronary heart disease (CHD) and also contribute to poorer health-related quality of life (HRQoL) and prognosis in patients with establishedCHD. PSRFs may also act as barriers to lifestyle changes and treatment adherence and may moderate the effects of cardiac rehabilitation (CR). Furthermore, there appears to be a bidirectional interaction between PSRFs and the cardiovascular system. Stress, anxiety and depression affect the cardiovascular system through immune, neuroendocrine and behavioural pathways. In turn, CHD and its associated treatments may lead to distress in patients, including anxiety and depression. In clinical practice, PSRFs can be assessed with single-item screening questions, standardised questionnaires, or structured clinical interviews. Psychotherapy and medication can be considered to alleviate any PSRF-related symptoms and to enhance HRQoL, but the evidence for a definite beneficial effect on cardiac endpoints is inconclusive. A multimodal behavioural intervention, integrating counselling for PSRFs and coping with illness should be included within comprehensive CR. Patients with clinically significant symptoms of distress should be referred for psychological counselling or psychologically focused interventions and/or psychopharmacological treatment. To conclude, the success of CR may critically depend on the interdependence of the body and mind and this interaction needs to be reflected through the assessment and management of PSRFs in line with robust scientific evidence, by trained staff, integrated within the core CR team.

Numerous 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., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Background: Psychological factors are important in the etiology and prognosis of coronary heart disease (CHD). Cardiac rehabilitation (CR) aims to reduce psychological distress, besides other somatic risk factors. Studies have shown that CR is effective in reducing psychological distress, but little is known about gender-specific outcome differences. Our objective was to examine whether women and men benefit equally from outpatient CR in terms of reduction in psychological distress and whether women show more impaired psychological health at baseline of CR than do men., Methods: We enrolled 441 CHD patients (mean age 58+/-11 years, 79.8% men) who underwent a 12-week outpatient CR program. Psychological dimensions, namely, anxiety, depression, vital exhaustion, social inhibition, and negative affect, were assessed at baseline and post-CR. Multivariate analysis of variance (MANOVA), controlling for age, disease severity, and exercise capacity, was applied to test for gender-specific differences at baseline and change between baseline and post-CR. In addition, gender-specific effect sizes were calculated for the change on psychological dimensions., Results: Women and men did not differ on any psychological measure at baseline of CR. The effect sizes show small to moderate treatment effects on the psychological dimensions assessed. Gender had a significant impact on change on the dimensions vital exhaustion (F=5.040(df=1), p<0.05) and social inhibition (F=5.74(df=1), p<0.05). Women showed larger change on social inhibition and smaller change on vital exhaustion than men., Conclusions: Women and men do not differ in the extent of psychological distress at baseline of CR, which could be explained also by the exclusion of highly distressed women from treatment. CR is less effective among women with regard to vital exhaustion and more effective with regard to social inhibition compared with men in a sample of low distressed patients.

Study Objective: This study examined differences in objective and subjective measures of sleep between caregivers and noncaregivers., Design: Cross-sectional design., Setting: All assessments were conducted within the home., Participants: Seventy-three community-dwelling spousal caregivers of patients with Alzheimer's disease and 40 noncaregiving controls., Measurements and Results: Subjects completed a semistructured interview on sociodemographics, cognitive status of the care recipient, self-reported sleep quality, and functional outcome. A polysomnogram was conducted. Caregivers of patients with moderate to severe Alzheimer's disease reported significantly more sleep problems (P<.05) and more functional impairment as a result of sleepiness than noncaregivers (P<.01). Objectively, older caregivers of those with moderate to severe Alzheimer's disease slept less than older noncaregivers (P<.05); there were no other significant differences in objective sleep measures. There was a main effect for age, with older caregivers and older noncaregivers having lower sleep efficiency, less slow-wave sleep, and more stage 1 sleep than younger caregivers and noncaregivers (P<.05)., Conclusions: This study suggests that nighttime sleep is shorter but not otherwise disrupted in caregivers of patients with moderate to severe Alzheimer's disease compared with noncaregivers, and the impact of caregiving on sleep disturbance may be most salient for older caregivers. It is possible that these older caregivers are more vulnerable to the effects of sleep disruption and thus have trouble falling back to sleep when the time is afforded them. Future work is needed to examine the differences in care practices in caregivers by age and dementia severity. Perhaps more importantly, studies examining the health consequences of shortened sleep in this group are needed.

Background: The chronic stress of providing care for a spouse suffering from Alzheimer's disease has been associated with an increased risk for coronary artery disease and overall mortality. Procoagulant changes are kindled by mental stress, and they are prospectively associated with atherothrombotic events., Objective: To examine whether dementia caregivers would show greater coagulation activity and less fibrinolytic capacity than noncaregiving controls., Methods: Subjects were 48 (30 female and 18 male) elderly (mean age +/- SD, 72 +/- 9 years) community-dwelling spousal Alzheimer caregivers and 20 noncaregiving age- and gender-matched controls. Plasma levels of thrombin-antithrombin III, fibrin D-dimer, von Willebrand factor, tissue-type plasminogen activator, and plasminogen activator inhibitor 1 were measured., Results: D-dimer, a marker of fibrin formation and degradation, was significantly higher in caregivers than in controls (688 +/- 575 vs. 406 +/- 157 ng/ml, p = 0.021). Plasma levels of the four other hemostasis variables were not significantly different between the two groups. Controlling for the classic cardiovascular risk factors body mass index, hypertension status, smoking status, hypercholesterolemia, type II diabetes, and medication potentially affecting hemostasis did not change results., Conclusion: The findings suggest that Alzheimer caregivers have an increased fibrin turnover as compared to noncaregiving controls independent of common confounders of hemostasis. Such an elevated clotting diathesis might contribute to increased cardiovascular risk and overall mortality with dementia caregiving strain., (Copyright (c) 2005 S. Karger AG, Basel)

A hypercoagulable state might contribute to increased atherothrombotic risk in hypertension. The sympathetic nervous system is hyperactive in hypertension, and it regulates hemostatic function. We investigated the effect of nonspecific beta-adrenergic stimulation (isoproterenol) and blockade (propranolol) on clotting diathesis in hypertension. Fifteen hypertensive and 21 normotensive subjects underwent isoproterenol infusion in two sequential, fixed-order doses of 20 and then 40 ng. kg(-1). min(-1) for 15 min/dose. Thirteen subjects were double-blind studied after receiving placebo or propranolol (100 mg/day) for 5 days each. In hypertensive subjects, isoproterenol elicited a dose-dependent increase in plasma von Willebrand factor (vWF) antigen [F(2,34) = 5.02; P = 0.032] and a decrease in D-dimer [F(2,34) = 4.57; P = 0.040], whereas soluble tissue factor remained unchanged. Propranolol completely abolished the increase in vWF elicited by isoproterenol [F(1,12) = 10.25; P = 0.008] but had no significant effect on tissue factor and D-dimer. In hypertension, vWF is readily released from endothelial cells by beta-adrenergic stimulation, which might contribute to increased cardiovascular risk. However, beta-adrenergic stimulation alone may not be sufficient to trigger fibrin formation in vivo.