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Positive psychological well-being (PPWB) is increasingly recognized as a critical factor in cardiovascular health of both healthy individuals and those with cardiovascular diseases (CVD). This mini-review synthesizes the current state of knowledge on the relationship between PPWB and cardiovascular health, examining relevant studies on PPWB in both populations. The conceptualization of PPWB encompasses hedonic and eudaimonic facets, with constructs such as optimism, purpose in life, and vitality playing crucial roles. Studies among healthy individuals show a significant association between PPWB and improved cardiovascular health indicators, while research among cardiac patients highlights the importance of PPWB in predicting outcomes such as mortality and rehospitalization. Mechanistic pathways linking PPWB and cardiovascular health include biological processes, health behavior changes, and additional psychological resources that mitigate stress. Despite the growing evidence, questions remain unanswered, necessitating further research to understand these relationships and develop effective interventions. Promoting psychological well-being alongside physical health can enhance cardiovascular disease prevention and management, offering a comprehensive approach to improving patient outcomes and overall well-being.

BackgroundImplantable Cardioverter-Defibrillator (ICD) implantation is a life-saving intervention for individuals at risk of life-threatening arrhythmias. However, the psychosocial impact of ICD implantation extends beyond its cardiovascular benefits, potentially influencing emotional well-being and sexual health. This can lead to erectile dysfunction, which, is often associated with alexithymia. Both erectile dysfunction and alexithymia can significantly affect the psychological well-being of both patients and their partners.AimsThis study examines the association of erectile dysfunction with alexithymia in patients after ICD implantation. Additionally, we investigate potential moderators of this association.MethodPatients (N=165) completed self-rating questionnaires: Toronto Alexithymia scale (TAS-20), International Index of Erectile Function (IIEF-5), Adjustment disorder – new module (ADNM-20). Descriptive statistics, correlations, multivariate linear regressions, and moderation analysis were conducted.ResultsThe determinants of erectile dysfunction in ICD patients were explored in a regression model explaining 22% of the total variance. The ADNM-20 subscale preoccupation was found to significantly moderate the relationship between the alexithymia subscale externally oriented thinking and erectile dysfunction (R2 = 0.02, p=0.03).ConclusionWe did not find evidence for a relationship between externally oriented thinking and erectile dysfunction at low to average levels of preoccupation. However, evidence for such a relationship was found at high levels of preoccupation, where more externally oriented thinking was related to more erectile dysfunction. The intersection of alexithymia and erectile dysfunction represents a promising avenue for future research, offering opportunities to unravel the intricate connections between emotional processing and sexual health. Enhancing insights into this relationship could lead to innovative interventions that address the needs of individuals struggling with both conditions, fostering improved emotional expression, intimate relationships, and sexual satisfaction.

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.

IntroductionAcute myocardial infarction (MI) is a potentially fatal condition, leading to high psychological distress and possibly resulting in the development of depressive symptoms and posttraumatic stress symptoms (PTSS). The aim of this study was to investigate the association of clusters of positive psychosocial factors (resilience, task-oriented coping, positive affect and social support) with both MI-induced depressive symptoms and PTSS, independent of demographic factors.MethodsWe investigated 154 consecutive patients with MI, 3 and 12 months after hospital discharge. All patients completed the short version of the German Resilience Scale, the Coping Inventory for Stressful Situations (CISS), the Enriched Social Support Inventory (ESSI) and the Global Mood Scale (GMS). The level of interviewer-rated MI-induced posttraumatic stress disorder (PTSD) symptoms at 3- and 12-months follow-up was evaluated through the Clinician-Administered PTSD Scale (CAPS). Depressive symptoms were assessed at 3- and 12-month follow-up with the Beck Depression Inventory (BDI-II).ResultsThree different clusters were revealed: (1) lonely cluster: lowest social support, resilience and average task-oriented coping and positive affect; (2) low risk cluster: highest resilience, task-oriented coping, positive affect and social support; (3) avoidant cluster: lowest task-oriented coping, positive affect, average resilience and social support. The clusters differed in depressive symptoms at 3 months (F = 5.10; p

There is a high prevalence of job burnout in physicians, impacting both the professional and personal levels. This study aimed to investigate whether physicians with burnout show specific pathological traits and facets of their personalities compared with healthy controls, according to the dimensional personality models in the ICD-11 and DSM-5. The role of perceived stress, anxiety, and depression were exploratively investigated regarding group differences. Male physicians (n = 60) were recruited into two groups (burnout vs. healthy). The Personality Inventory for the DSM-5 Brief Form Plus (PID5BF+) and the Maslach Burnout Inventory (MBI) were applied. The Wilcoxon rank-sum test (WRS) showed group differences in five of the six traits and in six of the seventeen facets of the PID5BF+. Multiple binary logistic regression, controlling for age, showed that deceitfulness (3.34 (1.36–9.35), p = 0.013) and impulsivity (10.20 (2.4–61.46), p = 0.004) significantly predicted burnout. Moreover, the WRS showed significant group differences in perceived stress, depressive, and anxiety symptoms (all p < 0.00)]. The findings suggest a relationship between pathological personality facets and burnout in a sample of male physicians. In particular, the facets of deceitfulness and impulsivity appear to play an important role. Furthermore, burnout showed well-known associations with perceived stress, depressive, and anxiety symptoms.

Background: Physician burnout, characterized by chronic job-related stress leading to emotional exhaustion, depersonalization, and reduced personal accomplishment. This cross-sectional study investigates cortisol reactivity in male physicians with burnout compared to healthy controls during an acute psychosocial stress test. Methods: Sixty male physicians (30 burnout, 30 healthy controls) participated between September 2019 and December 2021 to investigate the impact of burnout on cardiovascular health. Salivary cortisol levels were measured before and after a Trier Social Stress Test (TSST). Burnout was assessed with the Maslach Burnout Inventory-Human Services Survey (MBI-HSS). Covariates included age, BMI, and physical activity. Data were analyzed using repeated measures analysis and area under the curve analysis. Results: Male physicians with burnout exhibited significantly greater cortisol reactivity during the TSST, notably post-stress to 15 min post-stress. Emotional exhaustion correlated with reduced cortisol increase from pre-stress and smaller post-stress to 15- and 45-min declines. Discussion: Findings suggest heightened cortisol reactivity in male physicians with burnout, possibly reflecting initial chronic stress stages. This study highlights the necessity for long-term research on cortisol’s influence on cardiovascular health and stress responses across diverse groups. Conclusions: The findings contribute to comprehending physiological responses in burnout-afflicted physicians, emphasizing cortisol reactivity’s pivotal role in stress-related research and its potential health implications, particularly within the burnout context.

Objective: A growing body of literature suggests a relationship between personality traits and posttraumatic stress disorder (PTSD) symptoms after acute coronary events (ACS). However, specific personality profiles have not been examined in patients after ACS. Thus, the aim of the present study was to examine personality profiles created from response patterns on the resilience, alexithymia and type D personality (TDP) scales and to examine associations with PTSD symptoms, symptom clusters and coping styles among a sample of ACS patients. Methods: A cluster analytic approach was utilized to identify risk profiles based on personality variables and a series of ANOVAs in 154 patients. Post hoc analyses were conducted to examine the relationship between each profile, and interviewer-rated PTSD symptoms and different coping styles. Results: The analyses indicated a three-cluster solution, including low- (high resilience, low alexithymia and non-TDP), medium- (average resilience, average alexithymia and non-TDP) and high-risk (low resilience, high alexithymia and TDP) profiles. Clusters differed significantly in all three coping subscales. At 3-month follow up, clusters differed significantly in all three PTSD subscales (re-experiencing, avoidance and hyperarousal). At 12-month follow up, the differences remained significant for the hyperarousal subscale only. Conclusions: The personality profiles identified and the respective associations to PTSD symptoms and coping strategies highlight the potential impact for the psychological adjustment following ACS.

Objective: Myocardial infarction (MI) results in mental health consequences, including depression and post-traumatic stress disorder (PTSD). The risk and protective factors of such mental consequences are not fully understood. This study examined the relation between MI severity and future mental health consequences and the moderating role of vagal nerve activity. Methods: In a reanalysis of data from the Myocardial Infarction-Stress Prevention Intervention (MI-SPRINT) study, 154 post-MI patients participated. MI severity was measured by the Killip Scale and by troponin levels. Depression and PTSD symptoms were assessed with valid questionnaires, both at 3 and 12 months. Vagal nerve activity was indexed by the heart rate variability (HRV) parameter of the root-mean square of successive R-R differences (RMSSD). Following multivariate analyses, the association between MI severity and distress was examined in patients with low and high HRV (RMSSD = 30 ms). Results: In the full sample, the Killip index predicted post-MI distress only at 3 months, while troponin predicted distress at 3- and 12-months post-MI. However, HRV moderated the effects of the Killip classification; Killip significantly predicted symptoms of depression and PTSD at 3- and 12-months post-MI, but only in patients with low HRV. Such moderation was absent for troponin. Conclusion: MI severity (Killip classification) predicted post-MI depression and PTSD symptoms, but only in patients with low HRV, suggesting that the vagal nerve is a partial protective (moderating) factor in the relation between Killip score and post-MI distress.

Ineffective coping is a risk factor for burnout among physicians, in whom the prevalence of burnout is high and has also increased in recent years. We examined in a cross-sectional study whether physicians with burnout show different coping styles compared with healthy controls. Male physicians (n = 60) were recruited into two groups (burnout vs. healthy). The Coping Inventory for Stressful Situations (CISS) and the Maslach Burnout Inventory (MBI) were applied. Wilcoxon rank-sum test showed group differences in two of the three coping styles, task-oriented and emotion-oriented, and also in one of the two subscales of the avoidance-oriented coping: social-diversion-oriented coping. Multiple binomial logistic regression, controlling for age, showed that lower task-oriented coping (OR = 0.38 (0.13 - 0.93), p = 0.048, d = 0.534) and lower social-diversion-oriented coping (OR = 0.33 (0.11 - 0.80), p = 0.024, d = 0.611) significantly predicted the burnout group. The findings suggest that male physicians with burnout differ from healthy controls in terms of less frequent utilization of effective coping styles. These findings could be explored for their utility in preventing burnout in future studies.

ObjectivePsychological consequences of myocardial infarction (MI) are substantial, as 4% of all MI patients develop posttraumatic stress disorder (PTSD) and 12% clinically relevant posttraumatic stress symptoms (PTSS). The study investigated the course and development within 12 months of MI-induced PTSS to gain novel insights in potentially delayed response to early trauma-focused counseling aimed at preventing the incidence of MI-induced PTSS.MethodsIn the MI-SPRINT two-group randomized controlled trial, 190 MI-patients were randomly allocated to receive 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 12-month follow-up.Results12-month follow-up of outcomes were available for 106 (55.8%) of 190 participants: In the entire sample, one patient (0·5%, 1/190) who received trauma-focused counseling developed full PTSD. There was no significant difference between trauma-focused counseling and stress counseling regarding total score of interviewer-rated PTSS (p > 0.05). The only group difference emerged in terms of more severe hyperarousal symptoms in the trauma-focused counseling group in the ITT analysis, but not in the completer analysis.ConclusionsNo benefits were found for trauma-focused counseling after 12 months when compared with an active control intervention. PTSD prevalence in the present study was low highlighting a potential beneficial effect of both interventions. Further studies are needed to determine the most accurate approach of counseling.

BackgroundAfter acute coronary syndrome (ACS), one in eight patients develops clinically significant symptoms of Post-traumatic stress disorder (PTSD). We hypothesized that changes in cardiac symptoms from 3 to 12 months after ACS are associated with changes in ACS-induced PTSD symptoms.MethodsAt 3 (n = 154) and/or 12 months (n = 106) post-ACS, patients (n = 156, mean age 59 years, 85% men) completed a clinical interview assessing chest tightness/pain (at rest and/or during exertion), heartbeat symptoms (heart palpitations, racing of heart, heart stumbling or skipping a beat) and PTSD symptoms during the prior 4 weeks. Random mixed regression models examined the association between the onset (or remission) from 3 to 12 months in cardiac symptoms with changes in PTSD symptoms, adjusting for a range of potential predictors of ACS-induced PTSD symptoms.ResultsThe onset of chest tightness/pain [estimate = 0.588, 95% confidence interval: 0.275, 0.090; p < 0.001] and of heartbeat symptoms [0.548 (0.165, 0.931); p = 0.005] from 3 to 12 months was independently associated with an increase in total PTSD symptoms. There were also independent associations between the onset of chest tightness/pain and heartbeat symptoms with an increase in PTSD symptom clusters. Specifically, the onset of chest tightness/pain showed associations with an increase in re-experiencing [0.450 (0.167, 0.733); p = 0.027] and avoidance/numbing [0.287 (0.001, 0.574); p = 0.049]. The onset of heartbeat symptoms showed associations with an increase in re-experiencing [0.392 (0.045, 0.739); p = 0.002], avoidance/numbing [0.513 (0.161, 0.864); p = 0.004] and hyperarousal [0.355 (0.051, 0.659); p = 0.022]. An increase in the total number of cardiac symptoms (score range 0–6) was also associated with an increase in total PTSD symptoms [0.343 (0.202, 0.484); p < 0.001]. Psychotherapy in the post-hospital period moderated the association between the change in heartbeat symptoms and the change in total PTSD symptoms [−0.813 (−1.553, −0.074); p = 0.031 for interaction]; the association between the onset of heart beat symptoms and an increase in total PTSD symptoms was weaker in patients who attended psychotherapy [0.437 (−0.178, 1.052); p = 0.16] than in those who did not [0.825 (0.341, 1.309); p < 0.001].ConclusionChanges in cardiac symptoms between 3 and 12 months after hospitalization are associated with changes in ACS-induced PTSD symptoms. ClinicalTrials.gov #NCT01781247.

Background Sleep disturbance has been associated with poor prognosis in patients with acute coronary syndrome (ACS). This study examined the course of sleep disturbance and associated factors in patients with ACS who were followed for one year. Methods Study participants were 180 patients (mean age 59.6 years, 81.7% men) with ACS admitted to a tertiary hospital to undergo acute coronary intervention. Sleep disturbance was interviewer-assessed at admission (n = 180), at 3 months (n = 146), and at 12 months (n = 101) using the Jenkins Sleep Scale (JSS)-4, with a total of 414 assessments over one year. Random linear mixed regression models were used to evaluate the relationship between sociodemographic factors, cardiac diseases severity, perceived distress during ACS, comorbidities, medication, health behaviors, and sleep disturbance over time. Results At admission, 3 months, and 12 months, 56.7%, 49.3%, and 49.5% of patients, respectively, scored above the mean value for sleep disturbance in the general population (JSS-4 score ≥5). There was a significant decrease in continuous JSS-4 scores over time [estimate (SE) = -0.211 (0.074), p = 0.005]. Female sex [0.526 (0.206), p = 0.012], greater fear of dying [0.074 (0.026), p = 0.004], helplessness during ACS [0.062 (0.029), p = 0.034], and a history of depression [0.422 (0.171), p = 0.015] were independently associated with higher JSS-4 scores over time. Conclusion Despite a decrease from admission to 3 months, sleep disturbance is prevalent in the first year after ACS. Female sex, depression history, and distress during ACS identify patients at increased risk of developing persistent sleep disturbance and may inform interventions to prevent sleep disturbance.

Objective: Takotsubo syndrome (TTS) is characterized by transient left ventricular dysfunction, often elevated myocardial enzymes, and electrocardiographic changes. Previous studies suggested that an overstimulation of the sympathetic nervous system might cause TTS. However, the pathogenesis of TTS is largely unknown. Therefore, we investigated physiological stress reactivity with a standardized stress test in monozygotic twin sisters, only one of whom had experienced TTS. Methods: The 60-year-old Caucasian monozygotic twins, one with and one without a previous episode of TTS, were recruited in the Department of Cardiology at the University Hospital Zurich, Switzerland. We applied the Trier Social Stress Test (TSST) to investigate stress reactivity six weeks after the TTS. Hemodynamic measures (heart rate (HR), blood pressure (BP)), heart rate variability (HRV), plasma norepinephrine and epinephrine and salivary cortisol levels were collected immediately before and after the TSST, and 15, 45, and 90 min after TSST. The monozygotic twins differed in their hemodynamic stress response with the TTS twin showing blunted HR and BP reactivity and vagal withdrawal beyond the acute phase of stress. In contrast, the TTS twin showed a higher catecholamine and cortisol stress response with a steady increase in norepinephrine during the recovery period from stress compared to her non-TTS twin sister. Conclusion: Large studies applying a case-control design are needed to confirm blunted hemodynamic reactivity, increased catecholamine reactivity, vagal withdrawal, and increased cortisol reactivity to stress in TTS. This may advance the knowledge of psychophysiological mechanisms in TTS.

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.

Background Benzodiazepines and morphine are given during acute coronary syndromes (ACSs) to alleviate anxiety and pain, and β‐blockers may also reduce pain. ACS may induce posttraumatic stress disorder (PTSD) symptoms (PTSS). When taken during trauma other than ACS, benzodiazepines increase the risk of PTSS, but it is unknown if benzodiazepines increase the risk of PTSS in ACS. We examined the effects of drug exposure during ACS on the development of PTSS. Methods and Results Study participants were 154 patients with a verified ACS. Baseline demographics, clinical variables, and psychological measures were obtained through a medical history, through a psychometric assessment, and from patient records, and used as covariates in linear regression analysis. Three months after ACS, the severity of PTSS was assessed with the Clinician‐Administered PTSD Scale. During ACS, 37.7% of patients were exposed to benzodiazepines, whereas 72.1% were exposed to morphine and 88.3% were exposed to β‐blockers, but only 7.1% were exposed to antidepressants. Eighteen (11.7%) patients developed clinical PTSD. Adjusting for all covariates, benzodiazepine use was significantly associated with the Clinician‐Administered PTSD Scale total severity score (unstandardized coefficient B [SE], 0.589 [0.274]; partial r=0.18; P=0.032) and the reexperiencing subscore (B [SE], 0.433 [0.217]; partial r=0.17; P=0.047). Patients exposed to benzodiazepines had an almost 4‐fold increased relative risk of developing clinical PTSD, adjusting for acute stress disorder symptoms (odds ratio, 3.75; 95% CI, 1.31–10.77). Morphine, β‐blockers, and antidepressants showed no predictive value. Conclusions Notwithstanding short‐term antianxiety effects during ACS, benzodiazepine use might increase the risk of ACS‐induced PTSS with clinical significance, thereby compromising patients' quality of life and prognosis. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT01781247.

Background It has been acknowledged that medical life-threatening experiences such as an acute myocardial infarction (MI) often lead to acute stress disorder symptoms (ASS), which in turn can result in the development of post-traumatic stress symptoms (PTSS). Previous studies have suggested an association between various traumatic experiences and alexithymia. The association of alexithymia with ASS and PTSS in patients with MI is elusive. Objectives The aim of this study was to examine the association of alexithymia with MI-induced ASS and PTSS in patients at high risk of developing PTSD. Method Patients (N = 154) were examined twice, once within 48 hours, and then again three months after acute MI. All patients completed the self-rating Acute Stress Disorder Scale (ASDS) within 48 hours after the cardiac event. Three months after hospital discharge, all patients completed the Toronto Alexithymia Scale (TAS-20) and underwent the Clinician-Administered PTSD Scale (CAPS), a structured interview to assess the severity of PTSS. Descriptive statistics, correlations, multivariate linear regressions, and moderation analysis were conducted. Results The linear regression model explained 23% of the variance in MI-induced PTSS-symptoms (F(6.109) = 5.58, p 0.05). Conclusion In MI patients with high levels of DIF, ASS predicted the development of PTSS. If replicated, the finding may inform emotion-oriented interventions to investigate whether increasing the capacity to identify feelings following acute MI could be beneficial in preventing the development of PTSS.

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.

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.

Objective: Decreased heart rate variability (HRV) has been reported to be a predictor of mortality after myocardial infarction (MI). Patients’ beliefs and perceptions concerning their illness may play a role in decreased HRV. This study investigated if illness perceptions predict HRV at three months following acute MI. Methods: 130 patients referred to a tertiary cardiology centre, were examined within 48 hours and three months following acute MI. At admission, patients’ cognitive representations of their MI were assessed using the German version of the self-rated Brief Illness Perception Questionnaire (Brief IPQ). At admission and after three months (follow-up), frequency and time domain measures of HRV were obtained from 5-min electrocardiogram (ECG) recordings during stable supine resting. Results: Linear hierarchical regression showed that the Brief IPQ dimensions timeline (β coefficient = -0.29; p = .044), personal control (β = 0.47; p = .008) and illness understanding (β = 0.43; p = .014) were significant predictors of HRV, adjusted for age, gender, baseline HRV, diabetes, beta-blockers, left ventricular ejection fraction (LVEF), attendance of cardiac rehabilitation, and depressive symptoms. Conclusions: As patients’ negative perceptions of their illness are associated with lower HRV following acute MI, a brief illness perception questionnaire may help to identify patients who might benefit from a specific illness perceptions intervention.

The aim of this study was to examine whether heart drawings of patients with acute myocardial infarction reflect acute distress symptoms and negative illness beliefs and predict posttraumatic stress symptoms 3 months post-myocardial infarction. In total, 84 patients aged over 18 years drew pictures of their heart. The larger the area drawn as damaged, the greater were the levels of acute distress ( r = 0.36; p