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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) induces clinically significant posttraumatic stress symptoms (PTSS) in 12% of patients. Subjective sleep problems are a risk factor for the development of PTSS, but this is underexplored in patients with ACS. Purpose To examine the association of insomnia symptoms with ACS-induced PTSS. Methods In this longitudinal study with 154 patients (all white, 84.4% male, mean age 58.7 years) with a verified ACS, insomnia symptoms were interviewer assessed at hospital admission and at 3 months, using the Jenkins Sleep Scale (JSS)-4. ACS-induced PTSS were assessed with the Clinician-Administered Posttraumatic Stress Disorder Scale 3 months after hospital admission. In multivariable linear models, insomnia symptoms were regressed on PTSS, adjusting for demographics, clinical variables, health behaviors, and psychological data, including cognitive depressive symptoms. Results Greater insomnia symptoms at admission (β = .165, p = .034), greater increase in insomnia symptoms from admission to 3 months (β = .233, p = .008), and greater insomnia symptoms at 3 months (β = .239, p = .002) were independently associated with more severe total PTSS at 3 months. Concerning the individual PTSS clusters, both insomnia symptoms at admission (β = .214, p = .007) and at 3 months (β = .213, p = .012) were independently associated with reeexperiencing symptoms. Removing sleep items from PTSS scores and excluding patients on antidepressants in two sensitivity analyses did not substantially change the results. Conclusions Insomnia symptoms could play an important role in the development and severity of ACS-induced PTSS. This relationship seems not simply explained by the fact that sleeping difficulties are inherent to the phenotype of posttraumatic stress disorder. Clinical Trial information NCT01781247.

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.

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: Acute coronary syndrome (ACS)-induced posttraumatic stress disorder (PTSD) and clinically significant PTSD symptoms (PTSS) are found in 4 and 12% of patients, respectively. We hypothesized that trauma-focused counseling prevents the incidence of ACS-induced PTSS. Methods: Within 48 h of hospital admission, 190 patients with high distress during ACS were randomized to a single-session intervention of either trauma-focused counseling or an active control intervention targeting the general role of stress in patients with heart disease. Blind interviewer-rated PTSS (primary outcome) and additional health outcomes were assessed at 3 months of follow-up. Trial results about prevalence were compared with data from previous studies on the natural incidence of ACS-induced PTSS/PTSD. Results: Intention-to-treat analyses revealed no difference in interviewer-rated PTSS between trauma-focused counseling (mean, 11.33; 95% Cl, 9.23-13.43) and stress counseling (9.88; 7.36-12.40; p = 0.40), depressive symptoms (6.01, 4.98-7.03, vs. 4.71, 3.65-5.77; p = 0.08), global psychological distress (5.15, 4.07-6.23, vs. 3.80, 2.60-5.00; p = 0.11), and the risk for cardiovascular-related hospitalization/all-cause mortality (OR, 0.67; 95% CI, 0.37-1.23). Self-rated PTSS indicated less beneficial effects with trauma-focused (6.54; 4.95-8.14) versus stress counseling (3.74; 2.39-5.08; p = 0.017). The completer analysis (154 cases) confirmed these findings. The prevalence rates of interviewer-rated PTSD (0.5%, 1/190) and self-rated PTSS were in this trial much lower than in meta-analyses and observation studies from the same cardiology department. Conclusions: Benefits were not seen for trauma-focused counseling when compared with an active control intervention. Nonetheless, in distressed ACS patients, individual, single-session, early psychological counseling shows potential as a means to prevent posttraumatic responses, but trauma-focused early treatments should probably be avoided.

Self-rated health (SRH) is independently associated with all-cause mortality and adverse cardiovascular outcomes in individuals with and without cardiovascular disease. We examined whether SRH relates to haemostatic factors of a hypercoagulable state with prognostic impact in patients admitted with acute myocardial infarction (MI). We assessed 190 patients (median age: 59 years; all Caucasian; 83% men) within 48 hours of an acute coronary intervention in terms of demographic factors, medical and psychiatric comorbidity, health behaviours, cardiac-related variables and psychosocial characteristics. Patients rated their health state before MI retrospectively with the EuroQol Visual Analogue Scale ranging from 0 (‘worst imaginable health state’) to 100 (‘best imaginable health state’). Circulating levels of fibrinogen, fibrin D-dimer and von Willebrand factor (VWF) antigen were measured the morning after hospital referral. The median score of SRH was 75 (range: 20–100). SRH was inversely associated with fibrinogen (r = − 0.25, p = 0.001) and D-dimer (r = − 0.17, p = 0.021) levels in the bivariate analysis. Stronger relationships emerged for fibrinogen (r = − 0.33, p

Objective: Pain and inflammation during acute myocardial infarction (AMI) have been associated with the development of posttraumatic stress disorder and may also impact negatively on somatic outcome. We investigated the relationship between pain during AMI and levels of circulating proinflammatory (tumor necrosis factor [TNF]-α, interleukin [IL]-6) and anti-inflammatory (IL-33 and tissue growth factor [TGF]-β1) cytokines. Methods: Data were collected as part of the Myocardial Infarction - Stress Prevention Intervention (MI-SPRINT) study. We included 140 patients (mean age 59.6 years, 82.1% male) with high acute psychological distress within 48 h after MI. Fasting blood samples were drawn thereafter to measure cytokine levels. Sociodemographic factors, psychological and medical data, as well as cardiometabolic markers were assessed with questionnaires and patient interviews. Results: Linear regression models showed a significant positive correlation of pain with TGF-β1 (b = 770.91, p = 0.031) and a significant inverse correlation of pain with IL-33 (b = -0.11, p = 0.015) after controlling for age, gender, body mass index, lifetime depression, acute stress disorder symptoms, and the prognostic Global Registry of Acute Coronary Events (GRACE) score. Pain was not associated with IL-6 but with the GRACE score (b = 0.01, p = 0.003). Pain showed no significant association with TNF-α. Conclusion: Pain during MI was associated with anti- but not proinflammatory cytokines. As IL-33 has been shown to be cardioprotective, lower IL-33 levels with more intense pain may suggest a pathway through which increased pain during MI may have an impact on the medical prognosis.

Background: The aim of this study was to investigate the relationship between illness perception and posttraumatic stress disorder (PTSD) symptoms at three months following acute myocardial infarction (MI). Methods: Patients (n = 96) were examined within 48 h and 3 months after the illness episode. The brief revised illness perception questionnaire (Brief-IPQ) was used to assess patients' cognitive representation of their MI. At 3-month follow-up, the Posttraumatic Diagnostic Scale (PDS) and the Clinician-Administered PTSD Scale (CAPS) were used to assess the level of PTSD symptoms. Results: The subjective perception of the illness, including higher harmful consequences (r > 0.35, p < 0.01), higher illness concerns (r > 0.24, p < 0.05) and more emotional impairment (r > 0.23, p < 0.05), was associated with both self-rated and clinician-rated PTSD symptoms. Beliefs regarding harmful consequences after acute MI were independently associated with levels of PTSD symptoms assessed with both the self-rated PDS and CAPS interview (standardized beta coefficient = 0.24; P < 0.05) adjusted for demographic factors, cognitive depressive symptoms, fear of dying during MI, factors related to study design, and illness severity. Conclusions: The findings suggest that initial perception of acute MI is significantly associated with PTSD symptoms attributable to MI at 3 months follow-up.

Background Myocardial infarction-triggered acute stress disorder (ASD) and subclinical inflammation associate with the development of posttraumatic stress disorder, and worsen the prognosis of myocardial infarction patients. We examined the relationship between ASD severity and C-reactive protein levels in patients with acute myocardial infarction. Methods We assessed 190 patients (median age 59 years; 83% men) with a verified myocardial infarction within 48 h of an acute coronary intervention. Circulating levels of C-reactive protein were categorized according to their prognostic risk for cardiovascular disease: 0 to Results The ASDS sum score was positively associated with C-reactive protein categories in the bivariate analysis ( r = 0.20, p Conclusions Higher levels of myocardial infarction-triggered ASD symptoms associate with a greater inflammatory response in patients with acute myocardial infarction independently of important covariates. The findings suggest a link between myocardial infarction-triggered ASD symptoms and a heightened acute phase response with a potential impact on cardiovascular disease prognosis.

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.