18 research outputs found

    Unsichere BeschÀftigung und PrekaritÀt - im Lebensverlauf und im Haushalt

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    In diesem Kapitel werden auf der Basis von Mikrodaten Haushalts- und Familienstrukturen, BeschĂ€ftigungsverhĂ€ltnisse mit prekĂ€rem Potenzial und materielle Teilhabe aus der Querschnitts- und der Lebensverlaufsperspektive beschrieben. Im Mittelpunkt steht die Analyse des Zusammenhangs zwischen individuellen BeschĂ€ftigungsverhĂ€ltnissen mit prekĂ€rem Potenzial und materieller Teilhabe auf der Haushaltsebene. Über Sequenzmusteranalysen lassen sich Verlaufstypen mit dauerhafter gefĂ€hrdeter Teilhabe identifizieren, die auf prekĂ€re BeschĂ€ftigungsverlĂ€ufe und fehlende Sicherungsleistungen durch andere Haushaltsmitglieder zurĂŒckzufĂŒhren sind. Es werden insbesondere geschlechts- und regionsspezifische Unterschiede sichtbar

    Myoglobin for Detection of High-Risk Patients with Acute Myocarditis

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    There is an unmet need for accurate and practical screening to detect myocarditis. We sought to test the hypothesis that the extent of acute myocarditis, measured by late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR), can be estimated based on routine blood markers. A total of 44 patients were diagnosed with acute myocarditis and included in this study. There was strong correlation between myoglobin and LGE (rs = 0.73 [95% CI 0.51; 0.87], p < 0.001), while correlation was weak between LGE and TnT-hs (rs = 0.37 [95% CI 0.09; 0.61], p = 0.01). Receiver operating curve (ROC) analysis determined myoglobin ≄ 87 ÎŒg/L as cutoff to identify myocarditis (92% sensitivity, 80% specificity). The data were reproduced in an established model of coxsackievirus B3 myocarditis in mice (n = 26). These data suggest that myoglobin is an accurate marker of acute myocarditis. Graphical Abstract Receiver operating curve analysis determined myoglobin ≄ 87 ÎŒg/L as cutoff to identify myocarditis and these data were reproduced in an established model of coxsackievirus B3 myocarditis in mice: CMRI, cardiac magnetic resonance imaging; Mb, myoglobin; LGE, late gadolinium enhancement; ROC, receiver operating curve analysis

    A Novel Circulating MicroRNA for the Detection of Acute Myocarditis.

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    The diagnosis of acute myocarditis typically requires either endomyocardial biopsy (which is invasive) or cardiovascular magnetic resonance imaging (which is not universally available). Additional approaches to diagnosis are desirable. We sought to identify a novel microRNA for the diagnosis of acute myocarditis. To identify a microRNA specific for myocarditis, we performed microRNA microarray analyses and quantitative polymerase-chain-reaction (qPCR) assays in sorted CD4+ T cells and type 17 helper T (Th17) cells after inducing experimental autoimmune myocarditis or myocardial infarction in mice. We also performed qPCR in samples from coxsackievirus-induced myocarditis in mice. We then identified the human homologue for this microRNA and compared its expression in plasma obtained from patients with acute myocarditis with the expression in various controls. We confirmed that Th17 cells, which are characterized by the production of interleukin-17, are a characteristic feature of myocardial injury in the acute phase of myocarditis. The microRNA mmu-miR-721 was synthesized by Th17 cells and was present in the plasma of mice with acute autoimmune or viral myocarditis but not in those with acute myocardial infarction. The human homologue, designated hsa-miR-Chr8:96, was identified in four independent cohorts of patients with myocarditis. The area under the receiver-operating-characteristic curve for this novel microRNA for distinguishing patients with acute myocarditis from those with myocardial infarction was 0.927 (95% confidence interval, 0.879 to 0.975). The microRNA retained its diagnostic value in models after adjustment for age, sex, ejection fraction, and serum troponin level. After identifying a novel microRNA in mice and humans with myocarditis, we found that the human homologue (hsa-miR-Chr8:96) could be used to distinguish patients with myocarditis from those with myocardial infarction. (Funded by the Spanish Ministry of Science and Innovation and others.).Supported by a grant (PI19/00545, to Dr. MartĂ­n) from the Ministry of Science and Innovation through the Carlos III Institute of Health–Fondo de InvestigaciĂłn Sanitaria; by a grant from the Biomedical Research Networking Center on Cardiovascular Diseases (to Drs. MartĂ­n, SĂĄnchez-Madrid, and Ibåñez); by grants (S2017/BMD-3671-INFLAMUNE-CM, to Drs. MartĂ­n and SĂĄnchez-Madrid; and S2017/BMD-3867-RENIM-CM, to Dr. Ibåñez) from Comunidad de Madrid; by a grant (20152330 31, to Drs. MartĂ­n, SĂĄnchez-Madrid, and Alfonso) from FundaciĂł La MaratĂł de TV3; by grants (ERC-2011-AdG 294340-GENTRIS, to Dr. SĂĄnchez-Madrid; and ERC-2018-CoG 819775-MATRIX, to Dr. Ibåñez) from the European Research Council; by grants (SAF2017-82886R, to Dr. SĂĄnchez-Madrid; RETOS2019-107332RB-I00, to Dr. Ibåñez; and SAF2017-90604-REDT-NurCaMeIn and RTI2018-095928-BI00, to Dr. Ricote) from the Ministry of Science and Innovation; by Fondo Europeo de Desarrollo Regional (FEDER); and by a 2016 Leonardo Grant for Researchers and Cultural Creators from the BBVA Foundation to Dr. MartĂ­n. The National Center for Cardiovascular Research (CNIC) is supported by the Carlos III Institute of Health, the Ministry of Science and Innovation, the Pro CNIC Foundation, and by a Severo Ochoa Center of Excellence grant (SEV-2015-0505). Mr. Blanco-DomĂ­nguez is supported by a grant (FPU16/02780) from the FormaciĂłn de Profesorado Universitario program of the Spanish Ministry of Education, Culture, and Sports. Ms. Linillos-Pradillo is supported by a fellowship (PEJD-2016/BMD-2789) from Fondo de GarantĂ­a de Empleo Juvenil de Comunidad de Madrid. Dr. Relaño is supported by a grant (BES-2015-072625) from Contratos Predoctorales Severo Ochoa para la FormaciĂłn de Doctores of the Ministry of Economy and Competitiveness. Dr. Alonso-Herranz is supported by a fellowship from La Caixa–CNIC. Dr. Caforio is supported by Budget Integrato per la Ricerca dei Dipartimenti BIRD-2019 from UniversitĂ  di Padova. Dr. Das is supported by grants (UG3 TR002878 and R35 HL150807) from the National Institutes of Health and the American Heart Association through its Strategically Focused Research Networks.S

    Systematic use of cardiac magnetic resonance imaging in MINOCA led to a five-fold increase in the detection rate of myocarditis: a retrospective study

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    BACKGROUND Systematic work-up of patients with myocardial infarction and non-obstructive coronary artery disease (MINOCA) using cardiac magnetic resonance imaging (CMR) led to a more than six-fold increase in the detection rate of myocarditis. In this study, we expanded on our prior two-year analysis by including preceding and subsequent years. METHODS We performed a retrospective chart review of patients with angina-like symptoms and elevated high-sensitivity troponin T (TnT-hs &ge;14 ng/l) but without significant coronary artery disease, from 2011 to 2017. Patients underwent CMR to test for myocarditis. From 2011 to 2015, only patients with elevated TnT-hs, no significant coronary artery disease and moderate to high clinical likelihood of suffering from myocarditis, underwent CMR. In 2016 and 2017, CMR images were obtained from all patients with MINOCA, independent of the clinical likelihood that patients were suffering from myocarditis. RESULTS A total of 556 patients who underwent CMR (70.5% male, 57 &plusmn; 17 years, with an average left ventricular ejection fraction of 51 &plusmn; 15%) qualified for inclusion in this study&rsquo;s analysis. From 2011 to 2015, 240 CMR examinations were performed, with the number increasing to 316 between 2016 and 2017. In total, myocarditis was diagnosed in 76 out of the 556 patients (13.7%). Between 2011 and 2015, the detection rate of myocarditis was 12.7 per 100,000 hospitalisations and increased 4.9-fold (p &lt;0.0001), to 62.5 per 100,000 hospitalisations, between 2016 and 2017. CONCLUSION A novel diagnostic algorithm led to an average 4.9-fold increase in the rate of myocarditis detection in our hospital over the two subsequent years. This highlights that myocarditis continues to be underdiagnosed when CMR is not systematically used in patients with MINOCA. &nbsp

    Clinical Presentation and Laboratory Findings in Men Versus Women with Myocarditis

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    Objectives: Understanding sex differences in myocarditis is crucial to improve clinical care. We sought to investigate sex differences focusing on clinical presentation and laboratory parameters. Methods: From 2011 to 2018, 77 patients were diagnosed with myocarditis according to European Society of Cardiology (ESC) criteria with available clinical, laboratory, and cardiac magnetic resonance imaging data. First, we investigated sex differences of clinical and laboratory parameters in the entire cohort of 77 patients. Second, we focused on patients with acute myocarditis (n = 51) defined as recent symptom onset (≀10 days). Results: Myocarditis was present in 63 men (82%) and 14 women (18%). While men most frequently presented with chest pain (78%), a considerable amount of women presented with dyspnea as the only symptom (40%). Within the entire cohort, only creatinine kinase (CK) was higher in men versus women (364 ± 286 vs. 147 ± 148 U/L, p = 0.007), while in patients with acute myocarditis both CK and myoglobin (Mb) were higher in men versus women (CK: 327 ± 223 vs. 112 ± 65 U/L, p = 0.004 and Mb: 111 ± 126 vs. 25 ± 29 Όg/L, p = 0.04). No sex differences were found for high-sensitivity troponin T, C-reactive protein, and NT-probrain natriuretic peptide. Conclusions: This is the first study reporting sex differences in clinical presentation and routine laboratory parameters in myocarditis. While clinical presentation appeared to be subtle in women with dyspnea being the only presenting symptom of myocarditis in a considerable part, men typically complained of chest pain. Similarly to observations in myocardial infarction, atypical symptoms and underdiagnosis may be a cause for under-representation of women in cohorts of myocarditis

    Erysipelothrix rhusiopathiae infection by geese to human transmission

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    Erysipelothrix rhusiopathiae transmission to human is often occupation-related, but in most cases, a detailed case history is missing. This case report is based on an interdisciplinary approach and includes a thorough medical record. A 58-year-old laboratory technician working on geese necropsy cut open her glove at a rib fragment of a goose and subsequently noticed a slowly progressive, reddish skin alteration in the particular region of the hand. Bacteriological investigations on the geese revealed septicaemia due to E. rhusiopathiae and therefore substantiated the diagnosis of the patient. The infectious agent could not be cultured from the patient; however, antibiotic susceptibility testing was performed using the goose isolate. An entire follow-up until full recovery of the patient was conducted. Zoonotic infections possibly have a significant impact on certain occupations. This case report analyses a rare but important zoonotic infection to create awareness of this in physicians caring for human patients

    Non-steroidal anti-inflammatory drug use in acute myopericarditis: 12-month clinical follow-up

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    Objective Clinical data on the effect of non-steroidal anti-inflammatory drugs (NSAIDs) in myopericarditis are limited. Since NSAIDs are standard therapy in pericarditis, we retrospectively investigated their safety in myopericarditis. Methods In a retrospective case-control study, we identified 60 patients with myopericarditis from September 2010 to August 2017. Diagnosis was based on clinical criteria, elevated high-sensitivity troponin T and cardiac magnetic resonance imaging (CMR). All patients received standard heart failure therapy if indicated. Twenty-nine patients (62%) received NSAIDs (acetylsalicylic acid: n=7, average daily dose =1300 mg or ibuprofen: n=22, average daily dose =1500 mg) for an average duration of 4 weeks. To create two cohorts with similar baseline conditions, 15 patients were excluded. Three months after diagnosis, 29 patients were re-evaluated by CMR to measure late gadolinium enhancement (LGE). Results Baseline characteristics of those treated with or without NSAIDs were similar. Mean age was 34 (±13) years, 6 (13%) were women. Mean left ventricular ejection fraction (LVEF) was 56% (±5). 82 % of the patients (14 of 17) treated with NSAIDs experienced a decrease in LGE at 3 months, while it was only 58 % (7 of 12) of those without NSAIDs (p=0.15). At 12-month follow-up, one of the patients treated without NSAIDs experienced polymorphic ventricular tachycardia (VT) with cardiac arrest, while one of the patients with NSAIDs experienced non-sustained VT. Conclusions This is the first case-control study demonstrating that NSAIDs are safe in patients with myopericarditis and preserved LVEF. Our data suggest that this drug class should be tested prospectively in a large randomised clinical trial

    Myoglobin for Detection of High-Risk Patients with Acute Myocarditis

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    There is an unmet need for accurate and practical screening to detect myocarditis. We sought to test the hypothesis that the extent of acute myocarditis, measured by late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR), can be estimated based on routine blood markers. A total of 44 patients were diagnosed with acute myocarditis and included in this study. There was strong correlation between myoglobin and LGE (rs_{s} = 0.73 [95% CI 0.51; 0.87], p < 0.001), while correlation was weak between LGE and TnT-hs (rs_{s} = 0.37 [95% CI 0.09; 0.61], p = 0.01). Receiver operating curve (ROC) analysis determined myoglobin ≄ 87 Όg/L as cutoff to identify myocarditis (92% sensitivity, 80% specificity). The data were reproduced in an established model of coxsackievirus B3 myocarditis in mice (n = 26). These data suggest that myoglobin is an accurate marker of acute myocarditis. Graphical Abstract Receiver operating curve analysis determined myoglobin ≄ 87 Όg/L as cutoff to identify myocarditis and these data were reproduced in an established model of coxsackievirus B3 myocarditis in mice: CMRI, cardiac magnetic resonance imaging; Mb, myoglobin; LGE, late gadolinium enhancement; ROC, receiver operating curve analysis
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