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Background After an acute myocardial infarction (MI 2 ), patients may develop posttraumatic stress disorder (PTSD 3 ). There is evidence for alterations in the hypothalamic–pituitary–adrenal axis in PTSD. An association between patients` cortisol level after experiencing an MI and subsequent PTSD symptoms has not been investigated yet. Therefore, the aim of this study was to examine whether serum cortisol measured in patients admitted to hospital for acute coronary care after MI is predictive of PTSD symptoms at three and 12 months post-MI, respectively. Methods Patients (N=106) with a verified MI and high risk for the development of MI-induced PTSD symptoms were included in the study within 48 hours of hospital admission for acute coronary intervention. Serum cortisol was measured from fasting venous blood samples the next morning. Hierarchical regression analysis was used to test for an independent contribution of cortisol levels from admission to the Clinician-Administered PTSD Scale sum score three and 12 months after discharge from the coronary care unit. Results Hierarchical regression analysis showed that lower serum cortisol levels were significantly associated with more severe PTSD symptoms three months (B=-0.002, p=0.042) and 12 months (B=-0.002, p=0.043) post-MI. Limitations The generalizability of the findings is limited to patients with high acute peri-traumatic distress and without an acute severe depressive episode. The study does not provide any information about the diurnal cortisol pattern. Conclusion Lower serum cortisol measured during MI hospitalization may predict more severe MI-induced PTSD symptoms three and 12 months after hospital discharge.

BACKGROUND: Acute coronary syndrome (ACS) may cause clinically relevant posttraumatic stress disorder symptoms (PTSS). An inflammatory state might be one mechanism linking PTSS with poor prognosis after ACS. We tested the hypothesis that a change in C-reactive protein (CRP) between hospital admission and 3-month follow-up is an independent predictor of ACS-triggered PTSS. METHODS: We assessed 183 patients (median age 59 years; 84% men) with verified myocardial infarction (MI) within 48 h of an acute coronary intervention and three months post-MI for self-rated PTSS. 14 (7.7%) patients fulfilled definition criteria for PTSS caseness. CRP values were categorized according to the predicted risk of cardiovascular disease (CVD) at hospital admission (acute inflammatory response): 0 to

Background: Sleep problems predict incident cardiovascular events and mortality. Whether sleep also affects cardiovascular prognosis and through which mechanisms is less clear. We evaluated the relationship of a clinical risk of obstructive sleep apnea (OSA) and insomnia symptoms with neuroendocrine and coagulation activity in patients with acute myocardial infarction. Methods: Within 48 h of an acute coronary intervention, 190 patients (mean age 60 years, 82.6% male) were interviewed to assess OSA risk (STOP screening tool) and sleep difficulties (Jenkins Sleep Scale). Concentrations of epinephrine, norepinephrine, cortisol, fibrinogen, D-dimer, and von Willebrand factor were measured in plasma/serum. Multivariate models linking sleep to neuroendocrine and coagulation outcomes were controlled for demographic factors, health behaviors, comorbidity and cardiac-related variables, and mutually adjusted for OSA risk and sleep difficulties. Results: A high risk of OSA was identified in 40.5% of patients, and sleep difficulties on more than seven days in the previous four weeks were reported by 27.4% of patients. Compared to those with a low OSA risk, patients with a high OSA risk had lower epinephrine (p = 0.015), norepinephrine (p = 0.049) and cortisol (p = 0.001) levels, independently of covariates. More sleep difficulties were associated with higher fibrinogen (p = 0.037) and lower norepinephrine (p = 0.024) levels, with difficulties initiating, respectively maintaining sleep, driving these relationships. OSA risk was not significantly associated with coagulation activity. Conclusions: Sleep problems may relate to neuroendocrine and coagulation activity in patients with acute myocardial infarction. The pattern of relationships is not uniform for OSA and sleep difficulties and even varies between individual sleep difficulties.