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Background: In the hospital setting, frailty is a significant risk factor, but difficult to measure in clinical practice. We propose a reweighting of an existing diagnoses-based frailty score using routine data from a tertiary care teaching hospital in southern Germany., Methods: The dataset includes patient characteristics such as sex, age, primary and secondary diagnoses and in-hospital mortality. Based on this information, we recalculate the existing Hospital Frailty Risk Score. The cohort includes patients aged ≥ 75 and was divided into a development cohort (admission year 2011 to 2013, N = 30,525) and a validation cohort (2014, N = 11,202). A limited external validation is also conducted in a second validation cohort containing inpatient cases aged ≥ 75 in 2022 throughout Germany (N = 491,251). In the development cohort, LASSO regression analysis was used to select the most relevant variables and to generate a reweighted Frailty Score for the German setting. Discrimination is assessed using the area under the receiver operating characteristic curve (AUC). Visualization of calibration curves and decision curve analysis were carried out. Applicability of the reweighted Frailty Score in a non-elderly population was assessed using logistic regression models., Results: Reweighting of the Frailty Score included only 53 out of the 109 frailty-related diagnoses and resulted in substantially better discrimination than the initial weighting of the score (AUC = 0.89 vs. AUC = 0.80, p < 0.001 in the validation cohort). Calibration curves show a good agreement between score-based predictions and actual observed mortality. Additional external validation using inpatient cases aged ≥ 75 in 2022 throughout Germany (N = 491,251) confirms the results regarding discrimination and calibration and underlines the geographic and temporal validity of the reweighted Frailty Score. Decision curve analysis indicates that the clinical usefulness of the reweighted score as a general decision support tool is superior to the initial version of the score. Assessment of the applicability of the reweighted Frailty Score in a non-elderly population (N = 198,819) shows that discrimination is superior to the initial version of the score (AUC = 0.92 vs. AUC = 0.87, p < 0.001). In addition, we observe a fairly age-stable influence of the reweighted Frailty Score on in-hospital mortality, which does not differ substantially for women and men., Conclusions: Our data indicate that the reweighted Frailty Score is superior to the original Frailty Score for identification of older, frail patients at risk for in-hospital mortality. Hence, we recommend using the reweighted Frailty Score in the German in-hospital setting., (© 2024. The Author(s).)

Introduction: A rapid diagnosis of myocardial infarction (MI) is of utmost importance in order to provide adequate therapy for patients that suffer from acute ischemic cardiac injury. Cardiac troponin has evolved as the most significant biomarker in the diagnostic assessment of MI, but its evaluation and management can be challenging. Different troponin-based diagnostic protocols have been suggested for the diagnosis of MI and they have been validated and further developed over the years., Areas Covered: This review highlights the advances, characteristics, and challenges of rapid diagnostic protocols for MI and summarizes recent findings of investigations in the field., Expert Opinion: Although high-sensitivity troponin assays and rapid diagnostic protocols have revolutionized the assessment of suspected MI, we are still facing challenges that must be overcome in order to improve the outcome of patients with MI.

Background: In light of overlapping symptoms, discrimination between non-ST-elevation (NSTE) acute coronary syndrome (ACS) and acute heart failure (HF) is challenging, particularly in patients with equivocal clinical presentation for suspected ACS. We sought to evaluate the diagnostic and prognostic properties of copeptin in this scenario., Methods: Data from 1088 patients from a single-center observational registry were used to test the ability of serial high sensitivity cardiac troponin T (hs-cTnT)-compared to copeptin, or a combination of copeptin with hs-cTnT-to discriminate acute HF from uncomplicated non-ST-elevation myocardial infarction (NSTEMI) and to evaluate all-cause mortality after 365 days. Patients with STEMI, those with unstable angina and either normal or undetectable hs-cTnT concentrations were excluded. The findings were validated in an independent external NSTE-ACS cohort., Results: A total of 219 patients were included in the analysis. The final diagnosis was acute HF in 56 and NSTE-ACS in 163, with NSTEMI in 78 and unstable angina having stable elevation of hs-cTnT >ULN in 85. The rate of all-cause death at 1 year was 9.6% and occurred significantly more often in acute HF than in NSTE-ACS (15 vs. 6%, p < 0.001). In the test cohort, the area under the receiver operator curve (AUC) for the discrimination of acute HF vs. NSTE-ACS without HF was 0.725 (95% confidence interval [CI] 0.625-0.798) for copeptin and significantly higher than for hs-cTnT at 0 h (AUC = 0.460, 0.370-0.550) or at 3 h (AUC = 0.441, 0.343-0.538). Copeptin and hs-cTnT used either as continuous values or at cutoffs optimized to yield 90% specificity for acute HF were associated with significantly higher age- and sex-adjusted risk for all-cause mortality at 365 days. The findings from the test cohort were consistently replicated in the independent external NSTE-ACS validation cohort., Conclusions: High concentrations of copeptin in patients with suspected NSTE-ACS and equivocal clinical presentation suggest the presence of acute HF compared to uncomplicated NSTE-ACS and are associated with higher rates of all-cause death at 365 days.

Unlike classic synthetic stimulus-responsive and shape-memory materials, which remain limited to fixed responses, the responses of living systems dynamically adapt based on the repetition, intensity, and history of stimuli. Such plasticity is ubiquitous in biology, which is profoundly linked to memory and learning. Concepts thereof are searched for rudimentary forms of "intelligent materials." Here, we show plasticity of electroconductivity in soft ferromagnetic nickel colloidal supraparticles with spiny surfaces, assembling/disassembling to granular conducting micropillars between two electrodes driven by magnetic field B . Colloidal jamming leads to conduction hysteresis and bistable memory upon increasing and subsequently decreasing B . Abrupt B changes induce larger conduction changes than gradual B -changes. Periodic B pulsing drives to frequency-dependent facilitation or suppression of conductivity compared to exposing the same constant field. The concepts allow remotely controlled switching plasticity, illustrated by a rudimentary device. More generally, we foresee adaptive functional materials inspired by response plasticity and learning.

Background: While cardiac-specific troponin (cTn) allows for rapid diagnosis of acute type 1 myocardial infarction (T1MI), its performance to differentiate acute myocardial injury (AI) or type 2 myocardial infarction (T2MI) is limited. The objective was to combine biomarkers to improve discrimination of different myocardial infarction (MI) aetiologies., Methods: We determined levels of cardiac troponin T and I (cTnT, cTnI), cardiac myosin-binding protein C (cMyBP-C), NT-proBNP and ten miRNAs, known to be associated with cardiac pathology in a total of n = 495 serial plasma samples at three time points (on admission, after 1 h and 3 h) from 57 NSTEMI (non-ST-elevation myocardial infarction), 18 AI, and 31 STEMI patients, as defined by fourth universal definition of MI (UDMI4) and 59 control individuals. We then applied linear mixed effects model to compare the kinetics of all molecules in these MI sub-types., Results: Established (cTnT, cTnI) and novel (cMyBP-C) cardiac necrosis markers failed in differentiating T1MI vs T2MI at early time points. All cardiac necrosis markers were higher in T1MI than in T2MI at 3 h after admission. Muscle-enriched miRNAs (miR-1 and miR-133a) were correlated with cardiac necrosis protein markers and did not offer better discrimination. Established cardiac strain marker NT-proBNP differentiated AI and T1MI at all time points but failed to discriminate T2MI from T1MI. However, the combination of NT-proBNP and cTnT along with age returned an overall AUC of 0.76 [95 % CI 0.67-0.84] for differentiating T1MI, T2MI and AI., Conclusions: Rather than using single biomarkers of myocardial necrosis, a combination of clinical biomarkers for cardiac necrosis (troponin) and cardiac strain (NT-proBNP) might aid in differentiating T1MI, T2MI and AI., Competing Interests: M. Mayr is named inventor on a licensed patent held by King's College London for the detection of cMyBP-C as a biomarker of myocardial injury (EP2430453B1, US8546089). M. Mayr filed and licensed patent applications on miRNAs as biomarkers (EP15193448.6, EP2776580 B1, DE112013006129T5, GB2524692A, EP2576826 B, JP2013-513740). JT Neumann received honoraria from Siemens and Abbott Diagnostics. PMH reports fees from Beckman Coulter. D. Westermann reports personal fees from Bayer, Boehringer-Ingelheim, Berlin Chemie, Astra Zeneca, Biotronik and Novartis. S. Blankenberg received honoraria from Abbott Diagnostics, Siemens, Thermo Fisher, and Roche Diagnostics and is a consultant for Thermo Fisher., (© 2022 The Authors.)