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.

BackgroundObstructive 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.MethodsWe 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.ResultsHigh 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.ConclusionsIn 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 registrationClinicalTrials.gov NCT01781247.

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 β 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.

Acute coronary syndromes (ACS) induce post-traumatic stress symptoms (PTSS) in one out of eight patients. Effects of preventive interventions, the course and potential moderators of ACS-induced PTSS are vastly understudied. This study explored whether a preventive behavioral intervention leads to a decrease in myocardial infarction (MI)-induced PTSS between two follow-up assessments. Sociodemographic, clinical and psychological factors were additionally tested as both moderators of change over time in PTSS and predictors of PTSS across two follow-ups. Within 48 h after reaching stable circulatory conditions, 104 patients with MI were randomized to a 45-min one-session intervention of either trauma-focused counseling or stress counseling (active control). Sociodemographic, clinical, and psychological data were collected at baseline, and PTSS were assessed with the Clinician-Administered Post-traumatic Stress Disorder Scale 3 and 12 months post-MI. PTSS severity showed no change over time from 3 to 12 months post-MI, either in all patients or through the intervention [mean group difference for total PTSS = 1.6 (95% CI −1.8, 4.9), re-experiencing symptoms = 0.8 (95% CI −0.7, 2.2), avoidance/numbing symptoms = 0.1 (95% CI −1.6, 1.7) and hyperarousal symptoms = 0.6 (95% CI −0.9, 2.1)]. Patients receiving one preventive session of trauma-focused counseling showed a decrease from 3 to 12 months post-MI in avoidance symptoms with higher age (p = 0.011) and direct associations of clinical burden indices with total PTSS across both follow-ups (p's ≤ 0.043; interaction effects). Regardless of the intervention, decreases in re-experiencing, avoidance and hyperarousal symptoms from 3 to 12 months post-MI occurred, respectively, in men (p = 0.006), participants with low education (p = 0.014) and with more acute stress symptoms (p = 0.021). Peritraumatic distress (p = 0.004) and lifetime depression (p = 0.038) predicted total PTSS across both follow-ups. We conclude that PTSS were persistent in the first year after MI and not prevented by an early one-session intervention. A preventive one-session intervention of trauma-focused counseling may be inappropriate for certain subgroups of patients, although this observation needs confirmation. As predictors of the development and persistence of PTSS, sociodemographic and psychological factors could help to identify high-risk patients yet at hospital admission.