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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.

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.

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: 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. [ABSTRACT FROM AUTHOR]

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 FROM AUTHOR]

Background: A one-size-fits-all approach might explain why early psychological interventions are largely ineffective in preventing the development of posttraumatic stress disorder (PTSD) symptoms triggered by acute medical events. We examined the hypothesis that social and health care resources are moderators of an intervention effect. Methods: Within 48 h of hospital admission, 129 patients (mean age 58 years, 83% men) with acute coronary syndrome (ACS) self-rated their social support and were randomized to one single session of trauma-focused counseling (TFC) or stress-focused counseling (SFC) (active control intervention). Clinician-rated PTSD symptoms, use of cardiac rehabilitation (CR) and use of psychotherapy were assessed at 3 and 12 months. Random mixed regression multivariable models were used to analyze associations with PTSD symptoms over time. Results: TFC did not prevent ACS-induced PTSD symptom onset better than SFC; yet, there were significant and independent interactions between "intervention" (TFC or SFC) and social support (p = 0.013) and between "intervention" and duration of CR in weeks (p = 0.034). Patients with greater social support or longer participation in CR had fewer PTSD symptoms in the TFC group compared with the SFC group. The number of psychotherapy sessions did not moderate the intervention effect. Conclusions: Early psychological intervention after ACS with a trauma-focused approach to prevent the development of PTSD symptoms may be beneficial for patients who perceive high social support or participate in CR for several weeks. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: A prothrombotic tendency could partially explain the poor prognosis of patients with coronary heart disease and depression. We hypothesized that cognitive depressive symptoms are positively associated with the coagulation activation marker D‐dimer throughout the first year after myocardial infarction (MI). Methods: Patients with acute MI (mean age 60 years, 85% men) were investigated at hospital admission (n = 190), 3 months (n = 154) and 12 months (n = 106). Random linear mixed regression models were used to evaluate the relation between cognitive depressive symptoms, assessed with the Beck depression inventory (BDI), and changes in plasma D‐dimer levels. Demographics, cardiac disease severity, medical comorbidity, depression history, medication, health behaviors, and stress hormones were considered for analyses. Results: The prevalence of clinical depressive symptoms (13‐item BDI score ≥ 6) was 13.2% at admission and stable across time. Both continuous (p <.05) and categorical (p <.010) cognitive depressive symptoms were related to higher D‐dimer levels over time, independent of covariates. Indicating clinical relevance, D‐dimer was 73 ng/ml higher in patients with a BDI score ≥ 6 versus those with a score < 6. There was a cognitive depressive symptom‐by‐cortisol interaction (p <.05) with a positive association between cognitive depressive symptoms and D‐dimer when cortisol levels were high (p <.010), but not when cortisol levels were low (p >.05). Fluctuations (up and down) of cognitive depressive symptoms and D‐dimer from one investigation to the next showed also significant associations (p <.05). Conclusions: Cognitive depressive symptoms were independently associated with hypercoagulability in patients up to 1 year after MI. Hypothalamic–pituitary–adrenal axis could potentially modify this effect. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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]-a, interleukin [IL]-6) and anti-inflammatory (IL-33 and tissue growth factor [TGF]-ß 1) cytokines. Methods: Data were collected as part of the Myocardial Infarction - Stress Prevention Intervention (MISPRINT) 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. [ABSTRACT FROM AUTHOR]

Background and Objectives: After a previous report demonstrated blunted heart rate (HR) reactivity in association with adverse childhood experiences (ACEs) [Voellmin, A., Winzeler, K., Hug, E., Wilhelm, F. H., Schaefer, V., Gaab, J., … Bader, K. (2015). Blunted endocrine and cardiovascular reactivity in young healthy women reporting a history of childhood adversity. Psychoneuroendocrinology, 51, 58-67. doi: 10.1016/j.psyneuen.2014.09.008 ], the present analysis aimed at clarifying the role of the sympathetic and parasympathetic branches of the autonomic nervous system in this relationship.Design and Methods: One hundred eighteen healthy young women provided data on ACEs and underwent psychosocial stress testing. Systolic blood pressure (SBP) and respiratory sinus arrhythmia (RSA, quantified by high-frequency HR variability) were assessed as measures of sympathetic and parasympathetic cardiovascular activity, respectively. A mediation model was calculated to test the indirect effects of ACEs on HR via SBP and RSA.Results: The effect of ACEs on HR reactivity was mediated by SBP reactivity but not by RSA reactivity. ACEs were associated with reduced SBP at rest.Conclusions: ACEs were associated with down-regulation in a measure of sympathetic but no alteration in a measure of parasympathetic cardiovascular stress reactivity in adulthood. Future research will need to clarify whether this indicates risk or resilience. [ABSTRACT FROM AUTHOR]

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 3 months following acute MI. Methods: 130 patients referred to a tertiary cardiology center, were examined within 48 h and 3 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 3 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 = 0.044), personal control (β = 0.47; p = 0.008) and illness understanding (β = 0.43; p = 0.014) 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. [ABSTRACT FROM AUTHOR]

Background Posttraumatic Stress Disorder (PTSD) may occur in patients after exposure to a life-threatening illness. About one out of six patients develop clinically relevant levels of PTSD symptoms after acute myocardial infarction (MI). Symptoms of PTSD are associated with impaired quality of life and increase the risk of recurrent cardiovascular events. The main hypothesis of the MI-SPRINT study is that trauma-focused psychological counseling is more effective than non-trauma focused counseling in preventing posttraumatic stress after acute MI. Methods/design The study is a single-center, randomized controlled psychological trial with two active intervention arms. The sample consists of 426 patients aged 18 years or older who are at 'high risk' to develop clinically relevant posttraumatic stress symptoms. 'High risk' patients are identified with three single-item questions with a numeric rating scale (0 to 10) asking about 'pain during MI', 'fear of dying until admission' and/or 'worrying and feeling helpless when being told about having MI'. Exclusion criteria are emergency heart surgery, severe comorbidities, current severe depression, disorientation, cognitive impairment and suicidal ideation. Patients will be randomly allocated to a single 45-minute counseling session targeting either specific MI-triggered traumatic reactions (that is, the verum intervention) or the general role of psychosocial stress in coronary heart disease (that is, the control intervention). The session will take place in the coronary care unit within 48 hours, by the bedside, after patients have reached stable circulatory conditions. Each patient will additionally receive an illustrated information booklet as study material. Socio-demographic factors, psychosocial and medical data, and cardiometabolic risk factors will be assessed during hospitalization. The primary outcome is the interviewer-rated posttraumatic stress level at three-month follow-up, which is hypothesized to be at least 20% lower in the verum group than in the control group using the t-test. Secondary outcomes are posttraumatic stress levels at 12-month follow-up, and psychosocial functioning and cardiometabolic risk factors at both follow-up assessments. Discussion If the verum intervention proves to be effective, the study will be the first to show that a brief trauma-focused psychological intervention delivered within a somatic health care setting can reduce the incidence of posttraumatic stress in acute MI patients. [ABSTRACT FROM AUTHOR]