BACKGROUND: Collaboration for the Diagnosis and Evaluation of Acute Coronary Syndrome (CoDE-ACS) is a validated clinical decision support tool that uses machine learning with or without serial cardiac troponin measurements at a flexible time point to calculate the probability of myocardial infarction (MI). How CoDE-ACS performs at different time points for serial measurement and compares with guideline-recommended diagnostic pathways that rely on fixed thresholds and time points is uncertain. METHODS: Patients with possible MI without ST-segment–elevation were enrolled at 12 sites in 5 countries and underwent serial high-sensitivity cardiac troponin I concentration measurement at 0, 1, and 2 hours. Diagnostic performance of the CoDE-ACS model at each time point was determined for index type 1 MI and the effectiveness of previously validated low- and high-probability scores compared with guideline-recommended European Society of Cardiology (ESC) 0/1-hour, ESC 0/2-hour, and High-STEACS (High-Sensitivity Troponin in the Evaluation of Patients With Suspected Acute Coronary Syndrome) pathways. RESULTS: In total, 4105 patients (mean age, 61 years [interquartile range, 50–74]; 32% women) were included, among whom 575 (14%) had type 1 MI. At presentation, CoDE-ACS identified 56% of patients as low probability, with a negative predictive value and sensitivity of 99.7% (95% CI, 99.5%–99.9%) and 99.0% (98.6%–99.2%), ruling out more patients than the ESC 0-hour and High-STEACS (25% and 35%) pathways. Incorporating a second cardiac troponin measurement, CoDE-ACS identified 65% or 68% of patients as low probability at 1 or 2 hours, for an identical negative predictive value of 99.7% (99.5%–99.9%); 19% or 18% as high probability, with a positive predictive value of 64.9% (63.5%–66.4%) and 68.8% (67.3%–70.1%); and 16% or 14% as intermediate probability. In comparison, after serial measurements, the ESC 0/1-hour, ESC 0/2-hour, and High-STEACS pathways identified 49%, 53%, and 71% of patients as low risk, with a negative predictive value of 100% (99.9%–100%), 100% (99.9%–100%), and 99.7% (99.5%–99.8%); and 20%, 19%, or 29% as high risk, with a positive predictive value of 61.5% (60.0%–63.0%), 65.8% (64.3%–67.2%), and 48.3% (46.8%–49.8%), resulting in 31%, 28%, or 0%, who require further observation in the emergency department, respectively. CONCLUSIONS: CoDE-ACS performs consistently irrespective of the timing of serial cardiac troponin measurement, identifying more patients as low probability with comparable performance to guideline-recommended pathways for MI. Whether care guided by probabilities can improve the early diagnosis of MI requires prospective evaluation. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00470587.

Background: Aim of this study was to evaluate the outcomes of endocarditis patients undergoing valve surgery with the Cytosorb^® hemoadsorption (HA) device during cardiopulmonary bypass. Methods: From 2009 until 2019, 241 patients had undergone valve surgery due to endocarditis at the Department of Cardiac Surgery, University Hospital of Basel. We compared patients who received HA during surgery (n = 41) versus patients without HA (n = 200), after applying inverse probability of treatment weighting. Results: In-hospital mortality, major adverse cardiac and cerebrovascular events and postoperative renal failure were similar in both groups. Demand for norepinephrine (88.4 vs. 52.8%; p = 0.001), milrinone (42.2 vs. 17.2%; p = 0.046), red blood cell concentrates (65.2 vs. 30.6%; p = 0.003), and platelets (HA vs. Control: 36.7 vs. 9.8%; p = 0.013) were higher in the HA group. In addition, a higher incidence of reoperation for bleeding (34.0 vs. 7.7 %; p = 0.011), and a prolonged length of in-hospital stay (15.2 (11.8 to 19.6) vs. 9.0 (7.1 to 11.3) days; p = 0.017) were observed in the HA group. Conclusions: No benefits of HA-therapy were observed in patients with infective endocarditis undergoing valve surgery.

Cardiac myosin-binding protein C (cMyC) demonstrated high diagnostic accuracy for the early detection of non-ST-elevation myocardial infarction (NSTEMI). Its dynamic release kinetics may enable a 0/1h-decision algorithm that is even more effective than the ESC hs-cTnT/I 0/1 h rule-in/rule-out algorithm. In a prospective international diagnostic study enrolling patients presenting with suspected NSTEMI to the emergency department, cMyC was measured at presentation and after 1 h in a blinded fashion. Modelled on the ESC hs-cTnT/I 0/1h-algorithms, we derived a 0/1h-cMyC-algorithm. Final diagnosis of NSTEMI was centrally adjudicated according to the 4th Universal Definition of Myocardial Infarction. Among 1495 patients, the prevalence of NSTEMI was 17%. The optimal derived 0/1h-algorithm ruled-out NSTEMI with cMyC 0 h concentration below 10 ng/L (irrespective of chest pain onset) or 0 h cMyC concentrations below 18 ng/L and 0/1 h increase <4 ng/L. Rule-in occurred with 0 h cMyC concentrations of at least 140 ng/L or 0/1 h increase ≥15 ng/L. In the validation cohort (n = 663), the 0/1h-cMyC-algorithm classified 347 patients (52.3%) as ‘rule-out’, 122 (18.4%) as ‘rule-in’, and 194 (29.3%) as ‘observe’. Negative predictive value for NSTEMI was 99.6% [95% confidence interval (CI) 98.9–100%]; positive predictive value 71.1% (95% CI 63.1–79%). Direct comparison with the ESC hs-cTnT/I 0/1h-algorithms demonstrated comparable safety and even higher triage efficacy using the 0h-sample alone (48.1% vs. 21.2% for ESC hs-cTnT-0/1 h and 29.9% for ESC hs-cTnI-0/1 h; P < 0.001). The cMyC 0/1h-algorithm provided excellent safety and identified a greater proportion of patients suitable for direct rule-out or rule-in based on a single measurement than the ESC 0/1h-algorithm using hs-cTnT/I. ClinicalTrials.gov number, NCT00470587.

To directly compare the diagnostic accuracy of high-sensitivity cardiac troponin (hs-cTn) T vs. hs-cTnI in the early non-invasive differentiation of Type 1 myocardial infarction (T1MI) due to plaque rupture and atherothrombosis from Type 2 myocardial infarction (T2MI) due to supply–demand mismatch. In a prospective multicentre diagnostic study, two independent cardiologists centrally adjudicated the final diagnosis of T1MI vs. T2MI according to the fourth universal definition of myocardial infarction (MI), using all available clinical information including cardiac imaging in patients presenting with acute chest pain. Diagnostic accuracy was quantified by the area under the receiver operating characteristics curve (AUC). The most extensively validated hs-cTnT-Elecsys and hs-cTnI-Architect assays were measured at presentation, 1 h, and 2 h. Among 5887 patients, 1106 (19%) had a final diagnosis of MI, including 860 (78%) T1MI and 246 (22%) T2MI. The AUC of hs-cTnT-Elecsys to differentiate T1MI from T2MI was moderate and comparable to that provided by hs-cTnI-Architect: hs-cTnT-Elecsys AUC-presentation 0.67 [95% confidence interval (CI) 0.64–0.71], AUC-1 h 0.70 (95% CI 0.66–0.74), and AUC-2 h 0.71 (95% CI 0.66–0.75) vs. hs-cTnI-Architect AUC-presentation 0.71 (95% CI 0.67–0.74), AUC-1 h 0.72 (95% CI 0.68–0.76), and AUC-2 h 0.74 (95% CI 0.69–0.78), all P = not significant (NS). Similarly, the AUC of absolute changes was moderate and comparable for hs-cTnT-Elecsys and hs-cTnI-Architect (all P = NS). Cut-off concentrations achieving at least 90% specificity for the differentiation of T1MI vs. T2MI were >114 ng/L for hs-cTnT-Elecsys [odds ratio (OR) 4.2, 95% CI 2.7–6.6] and >371 ng/L for hs-cTnI-Architect (OR 4.0, 95% CI 2.6–6.2). hs-cTnT-Elecsys and hs-cTnI-Architect provided comparable, albeit only moderate, diagnostic accuracy for the early differentiation of T1MI vs. T2MI. ClinicalTrials.gov number, NCT00470587, https://clinicaltrials.gov/ct2/show/NCT00470587. Adjudicated diagnosis of acute chest pain patients and levels of hs-cTnT/I at presentation in T1MI and T2MI. Adjudicated diagnosis of T1MI and T2MI in patients presenting with acute chest pain to the emergency department and levels of hs-cTnT/I at presentation in both groups. hs-cTn, high-sensitivity cardiac Troponin; T1MI, type 1 myocardial infarction; T2MI, type 2 myocardial infarction.