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Abstract Background As a professional group, physicians are at increased risk of burnout and job stress, both of which are associated with an increased risk of coronary heart disease that is at least as high as that of other professionals. This study aimed to examine the association of burnout and job stress with coronary microvascular function, a predictor of major adverse cardiovascular events. Methods Thirty male physicians with clinical burnout and 30 controls without burnout were included. Burnout was assessed with the Maslach Burnout Inventory and job stress with the effort-reward imbalance and overcommitment questionnaire. All participants underwent myocardial perfusion positron emission tomography to quantify endothelium-dependent (cold pressor test) and endothelium-independent (adenosine challenge) coronary microvascular function. Burnout and job stress were regressed on coronary flow reserve (primary outcome) and two additional measures of coronary microvascular function in the same model while adjusting for age and body mass index. Results Burnout and job stress were significantly and independently associated with endothelium-dependent microvascular function. Burnout was positively associated with coronary flow reserve, myocardial blood flow response, and hyperemic myocardial blood flow (r partial = 0.28 to 0.35; p-value = 0.008 to 0.035). Effort-reward ratio (r partial = − 0.32 to − 0.38; p-value = 0.004 to 0.015) and overcommitment (r partial = − 0.30 to − 0.37; p-value = 0.005 to 0.022) showed inverse associations with these measures. Conclusions In male physicians, burnout and high job stress showed opposite associations with coronary microvascular endothelial function. Longitudinal studies are needed to show potential clinical implications and temporal relationships between work-related variables and coronary microvascular function. Future studies should include burnout and job stress for a more nuanced understanding of their potential role in cardiovascular health.

Abstract Background Obstructive sleep apnea (OSA) and insomnia are frequent sleep problems that are associated with poor prognosis in patients with coronary heart disease. The mechanisms linking poor sleep with an increased cardiovascular risk are incompletely understood. We examined whether a high risk of OSA as well as insomnia symptoms are associated with neuroendocrine hormones and coagulation factors in patients admitted with acute myocardial infarction. Methods We assessed 190 patients (mean age 60 years, 83% men) in terms of OSA risk (STOP screening tool for the assessment of high vs. low OSA risk) and severity of insomnia symptoms (Jenkins Sleep Scale for the assessment of subjective sleep difficulties) within 48 h of an acute coronary intervention. Circulating concentrations of epinephrine, norepinephrine, cortisol, fibrinogen, D-dimer, and von Willebrand factor were measured the next morning. The association of OSA risk and insomnia symptoms with neuroendocrine hormones and coagulation factors was computed using multivariate models adjusting for demographic factors, health behaviors, somatic and psychiatric comorbidities, cardiac disease-related variables, and OSA risk in the model for insomnia symptoms, respectively, for insomnia symptoms in the model for OSA risk. Results High OSA risk was identified in 41% of patients and clinically relevant insomnia symptoms were reported by 27% of patients. Compared to those with low OSA risk, patients with high OSA risk had lower levels of epinephrine (p = 0.015), norepinephrine (p = 0.049) and cortisol (p = 0.001). More severe insomnia symptoms were associated with higher levels of fibrinogen (p = 0.037), driven by difficulties initiating sleep, and with lower levels of norepinephrine (p = 0.024), driven by difficulties maintaining sleep. Conclusions In patients with acute myocardial infarction, sleep problems are associated with neuroendocrine hormones and coagulation activity. The pattern of these relationships is not uniform for patients with a high risk of OSA and those with insomnia symptoms, and whether they contribute to adverse cardiovascular outcomes needs to be established. Trial registration ClinicalTrials.gov NCT01781247.