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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.

PURPOSE Whether myocardial inflammation causes long-term sequelae potentially affecting myocardial blood flow (MBF) is unknown. We aimed to assess the effect of myocardial inflammation on quantitative MBF parameters, as assessed by 13N-ammonia positron emission tomography myocardial perfusion imaging (PET-MPI) late after myocarditis. METHODS Fifty patients with a history of myocarditis underwent cardiac magnetic resonance (CMR) imaging at diagnosis and PET/MR imaging at follow-up at least 6 months later. Segmental MBF, myocardial flow reserve (MFR), and 13N-ammonia washout were obtained from PET, and segments with reduced 13N-ammonia retention, resembling scar, were recorded. Based on CMR, segments were classified as remote (n = 469), healed (inflammation at baseline but no late gadolinium enhancement [LGE] at follow-up, n = 118), and scarred (LGE at follow-up, n = 72). Additionally, apparently healed segments but with scar at PET were classified as PET discordant (n = 18). RESULTS Compared to remote segments, healed segments showed higher stress MBF (2.71 mL*min-1*g-1 [IQR 2.18-3.08] vs. 2.20 mL*min-1*g-1 [1.75-2.68], p

Background After 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. Methods At 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. Results The 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]. Conclusion Changes 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.

Myocardial bridging (MB) is a segment of coronary arteries with an intramural course, typically spared from atherosclerosis, while the adjacent proximal segment is reported to be atherosclerosis-prone, a phenomenon contributed to local endothelial shear stress (ESS). We aimed to describe the ESS milieu in coronaries with MBs combining coronary computed tomography angiography with computational fluid dynamics and to investigate the association of atherosclerosis presence proximal to MBs with hemorheological characteristics. Patients ( n = 36) were identified and 36 arteries with MBs (11 deep and 25 superficial) were analyzed. ESS did not fluctuate 5 mm proximally to MBs vs 5 mm within MBs (0.94 vs 1.06 Pa, p = .56). There was no difference when comparing ESS in the proximal versus mid versus distal MB segments (1.48 vs 1.37 vs 1.9 Pa, p = ns). In arteries with plaques ( n = 12), no significant ESS variances were observed around the MB entrance, when analyzing all arteries ( p = .81) and irrespective of morphological features of the bridged segment (deep MBs; p = .65, superficial MBs; p = .84). MBs are characterized by homogeneous, atheroprotective ESS, possibly explaining the absence of atherosclerosis within bridged segments. The interplay between ESS and atherosclerosis is potentially not different in arteries with MB compared with arteries without bridges.

OBJECTIVE The traumatic experience of acute coronary syndrome (ACS) may induce symptoms of posttraumatic stress disorder (PTSD). We examined whether the ACS-triggered acute inflammatory response predicts the development of PTSD symptoms. METHOD Study participants were 70 patients (all Caucasian, 80% male, mean age 59��years) with myocardial infarction (MI) during the acute treatment phase. Interleukin (IL)-1��, IL-6, tumor necrosis factor (TNF)-��, IL-4, IL-10, and transforming growth factor (TGF)-1�� were determined in plasma collected within 48��h of hospital admission. Participants self-assessed the severity of ACS-induced PTSD symptoms with the 17-item Posttraumatic Diagnostic Scale at 12��months. RESULTS There was a significant positive association of the pro-inflammatory index (added standardized z-scores of pro-inflammatory cytokines IL-1��, IL-6, and TNF-��) with total PTSD symptom severity (��R2��=��0.050, p��=��.029) and re-experiencing symptoms (��R2��=��0.088, p��=��.008), but not avoidance/numbing and hyperarousal symptoms. Analyses were adjusted for the anti-inflammatory index (added standardized z-scores of IL-4, IL-10, and TGF-��1), trauma-focused counseling, sex, age, time since pain onset, troponin, body mass index, and distress during MI. Results were robust when the anti-inflammatory index was removed from the model. Additional analyses showed significant associations of both the net-inflammatory index (i.e., pro-inflammatory index minus anti-inflammatory index) and IL-1�� with total PTSD symptom severity, re-experiencing, and hyperarousal symptoms (��R2 between 0.042 and 0.090) and of IL-1�� with avoidance/numbing symptoms (��R2��=��0.050). CONCLUSIONS The findings suggest an association between the pro-inflammatory state launched during ACS and the development of PTSD symptoms. Increased IL-1�� may play a particular role in the pathophysiology of ACS-induced PTSD symptoms.

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.

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 ACSinduced PTSS with clinical significance, thereby compromising patients’ quality of life and prognosis.

Transthyretin amyloidosis (ATTR amyloidosis) is a disease caused by deposition of transthyretin fibrils in organs and tissues, which causes their dysfunction. The clinical heterogeneity of ATTR amyloidosis and the variable presentation of symptoms at early disease stages, historically meant treatment delays. Diagnostic tools and therapy options of ATTR amyloidosis have markedly improved in recent years. The first Swiss Amyloidosis Network (SAN) meeting (Zurich, Switzerland, January 2020) aimed to define a consensus statement regarding the diagnostic work-up and treatment for systemic amyloidosis, tailored to the Swiss healthcare system. A consortium of 45 clinicians and researchers from all Swiss regions and universities was selected by the SAN committee to represent all sub-specialty groups involved in care of patients with amyloidosis. A steering committee conducted the literature search and analysis, wrote the critical synthesis and elaborated a list of statements that were evaluated by all the participants. These recommendations will improve outcomes and quality of life for patients with ATTR amyloidosis. A global review of these guidelines is planned every 3 years with a formal meeting of all the involved experts.

OBJECTIVES We sought to assess the feasibility of prospective electrocardiogram triggering for achieving low dose computed tomography coronary angiography (CTCA) in a large population. BACKGROUND Prospective electrocardiogram triggering dramatically reduces radiation exposure for CTCA but requires heart rate (HR) control to obtain diagnostic image quality. Its feasibility in daily clinical routine has therefore remained to be elucidated. METHODS We evaluated 612 patients consecutively referred for CTCA by 64 slice computed tomography. Intravenous metoprolol (2 to 30 mg) was administered if necessary to achieve a target HR below 65 beats/min. Image quality was assessed on a semiquantitative 4 point scale for each coronary segment. RESULTS Forty six (7.5) patients were deemed ineligible due to irregular heart rhythm (n = 19) insufficient response to metoprolol (n = 21) renal insufficiency (n = 3) or inability to follow breath hold commands (n = 3). Mean effective radiation dose was 1.8 ± 0.6 mSv with a diagnostic image quality in 96.2 of segments. Finally low dose CTCA allowed a firm diagnosis with regard to the presence or absence of coronary artery disease in 527 (86.1) patients. Intravenous metoprolol to achieve an HR below 65 beats/min was used in 64.4 of patients. Incidence of nondiagnostic segments was inversely related to HR (r = 0.809 p < 0.001). Below an HR cutoff of 62 beats/min only 1.2 of coronary segments were nondiagnostic. CONCLUSIONS Low dose CTCA by electrocardiogram triggering is feasible in the vast majority of an every day population. However HR control is crucial as an HR below 62 beats/min favors diagnostic image quality.

BACKGROUND The outcome of patients with severe ischaemic left ventricular (LV) dysfunction is determined by the extent of myocardial viability and the presence of LV dyssynchrony. We aimed at assessing both parameters from the same imaging method i.e. gated positron emission tomography (PET) F18 fluorodeoxyglucose (FDG) scans. METHODS Phase analysis from Emory Cardiac Toolbox was applied on gated PET FDG scans to assess histogram bandwidth and standard deviation (SD) as a measure of LV dyssynchrony in 30 heart failure patients (mean ejection fraction: 30.2 ± 13.8) referred for the evaluation of myocardial viability. Cut off values from single photon emission computed tomography myocardial perfusion imaging (SPECT MPI) best predicting cardiac resynchronization therapy (CRT) response served as standard of reference (bandwidth

Objective The selective in vivo localization of antibody derivatives in atherosclerotic plaques may open novel diagnostic and therapeutic applications. Here, we present a comparative in vivo localization analysis of eight radioiodinated human monoclonal antibodies in apolipoprotein E-deficient (ApoE −/− ) mice. Methods Animals were fed with a cholesterol-rich diet, followed by harvesting of the aorta 24h after intravenous antibody injection and investigated by autoradiographic analysis. Localization of F8 antibody on atherosclerotic plaque structures was further studied in three-color fluorescence microscopy. Results The study revealed that the F8 antibody, specific to the alternatively spliced EDA domain of fibronectin, exhibited the highest plaque-targeting potential among the antibodies analyzed in this study, with an ability to preferentially localize to all plaques within the aorta. Targeting results were confirmed by injection of fluorescein-labeled F8 antibody, followed by three-color fluorescence microscopy analysis. Conclusion These findings open novel biomolecular avenues for the in vivo imaging of atherosclerotic plaques and for pharmacodelivery applications, since F8 had previously been reported by our group to strongly stain atherosclerotic plaques in human carotid arteries.

BACKGROUND Coronary computed tomography angiography (CCTA)-based transluminal attenuation gradient (TAG) was suggested to determine the functional significance of a stenosis. However, evidence that TAG acquired by wide-volume scanners can assess the hemodynamic significance of stenosis assessed by single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) is lacking. Moreover, coronary cross-sectional area may influence TAG. Hence, we aimed at assessing the diagnostic value of TAG to predict ischemia in SPECT-MPI and the correlation between TAG and the transluminal cross-sectional area gradient (TCG). METHODS Patients undergoing CCTA and SPECT-MPI for suspected coronary artery disease were included. TAG and TCG were calculated measuring the mean vessel attenuation and the cross-sectional area along major coronary vessels at 5-mm intervals. RESULTS A total of 255 coronary arteries of 87 patients were included. TAG and TCG did not discriminate between coronary arteries with or without ischemia as assessed by SPECT-MPI (p = .44 and p = .25, respectively). The area under the curve to predict ischemia was not increased by adding TAG (0.88, 95% CI 0.83-0.92) or TCG (0.87, 95% CI 0.81-0.90) to CCTA alone (0.85, 95% CI 0.80-0.89). There was a significant correlation between TAG and TCG (r = 0.43; p

Background Estimation of functional relevance of a coronary stenosis by fractional flow reserve (FFR) from coronary computed tomography angiography (CCTA) has recently provided encouraging results. Due to its limited availability, the corrected contrast opacification (CCO) decrease and the transluminal attenuation gradient (TAG) were suggested as less complex alternatives. The aim of the present study was to assess the accuracy of CCO decrease and TAG to predict ischemia as assessed by single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI). Results This retrospective study included 72 patients who underwent hybrid CCTA/SPECT MPI with at least one coronary artery stenosis. Of 127 vessels with a coronary stenosis in CCTA, 38 (30%) were causing ischemia in its subtending myocardium. The area under the curve (AUC) for CCO decrease to predict ischemia was 0.707 with sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of 74, 64, 85, 47, and 67%, respectively. For TAG, the AUC was 0.469. Conclusions CCTA-derived CCO decrease but not TAG predicts ischemia in SPECT MPI. The negative predictive value of CCO decrease of 85% may confer clinical implications in the diagnostic work-up of patients with a coronary stenosis.

BACKGROUND: Although randomized trials have provided evidence for invasive fractional flow reserve to guide revascularization, evidence for non-invasive imaging is less well established. The present study investigated whether hybrid coronary computed tomography (CCTA)/single photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) can identify patients who benefit from early revascularization compared to medical therapy. METHODS: This retrospective study consists of 414 patients referred for evaluation of known or suspected coronary artery disease (CAD) with CCTA/SPECT hybrid imaging. CCTA categorized patients into no CAD, non-high-risk CAD and high-risk CAD. In patients with CAD (n = 329), a matched finding (n = 75) was defined as a reversible perfusion defect in a territory subtended by a coronary artery with CAD. All other combinations of pathologic findings were classified as unmatched (n = 254). Death, myocardial infarction, unstable angina requiring hospitalization, and late coronary revascularization were defined as major adverse cardiac events (MACE). Cox hazards models included covariates age, male gender, more than two risk factors, previous CABG, high-risk CAD and early revascularization. RESULTS: During median follow-up of 6.0 years, 112 patients experienced a MACE (27%). Early revascularization (n = 50) was independently associated with improved outcome among patients with a matched finding (p