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Despite improved laboratory assays for cardiac markers and a revised standard for definition of myocardial infarction (AMI), early detection of coronary ischemia in unselected patients with chest pain remains a difficult challenge. Rapid measurements of troponin I (TnI), creatine kinase MB (CK-MB), and myoglobin were performed in 197 consecutive patients with chest pain and a nondiagnostic electrocardiogram for AMI. The early diagnostic performances of these markers and different multimarker strategies were evaluated and compared. Diagnosis of AMI was based on European Society of Cardiology/American College of Cardiology criteria. At a given specificity of 95%, TnI yielded the highest sensitivity of all markers at all time points. A TnI cutoff corresponding to the 10% coefficient of variation (0.1 μg/L) demonstrated a cumulative sensitivity of 93% with a corresponding specificity of 81% at 2 hours. The sensitivity was considerably higher compared to CK-MB and myoglobin, even considering patients with a short delay until admission. Using the 99th percentile of TnI results as a cutoff (0.07 μg/L) produced a cumulative sensitivity of 98% at 2 hours, but its usefulness was limited due to low specificities. Multimarker strategies including TnI and/or myoglobin did not provide a superior overall diagnostic performance compared to TnI using the 0.1 μg/L cutoff. A TnI cutoff corresponding to the 10% coefficient of variation was most appropriate for early diagnosis of AMI. A lower TnI cutoff may be useful for very early exclusion of AMI. CK-MB and in particular myoglobin did not offer additional diagnostic value.

BackgroundLong-term prognosis associated with low–high-sensitivity cardiac troponin T (hs-cTnT) concentrations in patients with chest pain is unknown. We investigated these prognostic implications compared with the general population.MethodsAll first visits to seven emergency departments (ED)s in Sweden were included from 9 December 2010 to 31 August, 2017 by patients presenting with chest pain and at least one hs-cTnT measured. Patients with myocardial injury (any hs-cTnT >14 ng/L), including patients with myocardial infarction (MI) were excluded. Standardised mortality ratios (SMRs) and standardised incidence ratios (SIRs) were calculated as the ratio of the number of observed to expected events. The expected number was computed by multiplying the 1-year calendar period-specific, age-specific and sex-specific follow-up time in the cohort with the corresponding incidence in the general population. HRs were calculated for all-cause mortality and major adverse cardiovascular events (MACE), defined as acute MI, heart failure hospitalisation, cerebrovascular stroke or cardiovascular death, between patients with undetectable (<5 ng/L) and low (5–14 ng/L) hs-cTnT.ResultsA total of 1 11 916 patients were included, of whom 69 090 (62%) and 42 826 (38%) had peak hs-cTnT concentrations of <5 and 5–14 ng/L. Patients with undetectable peak hs-cTnT had a lower mortality risk compared with the general Swedish population (SMR 0.83, 95% CI 0.79 to 0.87), with lower risks observed in all patients ≥65 years of age, but a slightly higher risk of being diagnosed with a future MI (SIR 1.39, 95% CI 1.32 to 1.47). The adjusted risk of a first MACE associated with low versus undetectable peak hs-cTnT was 1.6-fold (HR 1.61, 95% CI 1.53 to 1.70).ConclusionPatients with chest pain and undetectable hs-cTnT have an overall lower risk of death compared with the general population, with risks being highly age dependent. Detectable hs-cTnT concentrations are still associated with increased long-term cardiovascular risks.

AbstractIdentifying patients with chest pain that is of cardiac origin is crucial owing to the high mortality and morbidity of cardiovascular diseases. History, electrocardiogram, and cardiac biomarkers are the core elements of the assessment. High sensitivity cardiac troponins (hs-cTn) are the preferred biomarkers for diagnosing acute myocardial infarction, allowing for more accurate detection and exclusion of myocardial injury. However, elevations in hs-cTn can occur in patients who are not experiencing acute myocardial infarction. Therefore, it is important for clinicians to recognize how to integrate hs-cTn levels into their clinical decision making process. Structured risk assessments, using evidence based diagnostic protocols, should be employed to estimate the risk of acute coronary syndrome and adverse events in patients with chest pain. Clinical decision pathways should be used routinely in emergency departments. Patients at intermediate or high risk of obstructive coronary artery disease might benefit from cardiac imaging and further testing. Patients should be involved in decision making, with information provided about risks, radiation exposure, costs, and alternative options to facilitate informed decision making.

Clinical work-up for suspected cardiac chest pain is resource intensive. Despite expectations, high-sensitivity cardiac troponin assays have not made decision making easier. The impact of recently validated rapid triage protocols including the 0-hour/1-hour hs-cTn protocols on care and outcomes may be limited by the heterogeneity in interpretation of troponin profiles by clinicians. We have developed machine learning (ML) models which digitally phenotype myocardial injury and infarction with a high predictive performance and provide accurate risk assessment among patients presenting to EDs with suspected cardiac symptoms. The use of these models may support clinical decision-making and allow the synthesis of an evidence base particularly in non-T1MI patients however prospective validation is required. We propose that integrating validated real-time artificial intelligence (AI) methods into clinical care may better support clinical decision-making and establish the foundation for a self-learning health system. This prospective, multicenter, open-label, cluster-randomized clinical trial within blinded endpoint adjudication across 12 hospitals (n = 20,000) will randomize sites to the clinical decision-support tool or continue current standard of care. The clinical decision support tool will utilize ML models to provide objective patient-specific diagnostic probabilities (ie, likelihood for Type 1 myocardial infarction [MI] versus Type 2 MI/Acute Myocardial Injury versus Chronic Myocardial Injury etc.) and prognostic assessments. The primary outcome is the composite of cardiovascular mortality, new or recurrent MI and unplanned hospital re-admission at 12 months post index presentation. Supporting clinicians with a decision support tool that utilizes AI has the potential to provide better diagnostic and prognostic assessment thereby improving clinical efficiency and establish a self-learning health system continually improving risk assessment, quality and safety. ANZCTR, Registration Number: ACTRN12620001319965, https://www.anzctr.org.au/.

Acute post-streptococcal glomerulonephritis (APSGN) is the most common glomerulonephritis of childhood, and clinical presentation can vary widely. This case report presents an atypical manifestation of APSGN in an 8-year-old female patient with pleuritic chest pain and elevated troponin-I, despite lacking classical kidney symptoms. Imaging studies showed cardiomegaly and interstitial lung opacities. Further investigations revealed hematuria and proteinuria, and the diagnosis was confirmed through elevated antistreptolysin-O (ASO) titers and low complement 3 (C3) levels. The patient was successfully managed with fluid restriction, diuretics, and antihypertensives, resulting in the resolution of symptoms and normalization of laboratory values. This case highlights the significance of recognizing atypical manifestations of APSGN for ensuring prompt diagnosis and proper management in the pediatric population.

We evaluated kinetic changes of high-sensitivity cardiac troponin T (hs-cTnT) in patients with acute coronary syndrome (ACS) and patients with hs-cTnT increases not due to ACS to rule in or rule out non-ST-segment elevation myocardial infarction (STEMI). hs-cTnT was measured serially in consecutive patients presenting to the emergency department. Patients with ACS who had at least 2 hs-cTnT measurements within 6 h and non-ACS patients with hs-cTnT concentrations above the 99th percentile value (14 ng/L) were enrolled to compare absolute and relative kinetic changes of hs-cTnT. For discrimination of non-STEMI (n=165) in the entire study population (n=784), the absolute δ change with the ROC-optimized value of 9.2 ng/L yielded an area under the curve of 0.898 and was superior to all relative δ changes (P<0.0001). The positive predictive value for the absolute δ change was 48.7%, whereas the negative predictive value was 96.5%. In a specific ACS population with exclusion of STEMI (n=342), the absolute δ change with the ROC-optimized value of 6.9 ng/L yielded a positive predictive value of 82.8% and a negative predictive value of 93.0%. In comparison to the ≥20% relative δ change, the ROC-optimized absolute δ change demonstrated a significantly added value for the entire study population and for the ACS cohort (net reclassification index 0.331 and 0.499, P<0.0001). Absolute δ changes appear superior to relative δ changes in discriminating non-STEMI. A rise or fall of at least 9.2 ng/L in the entire study population and 6.9 ng/L in selected ACS patients seems adequate to rule-out non-STEMI. However, δ-values are useful to rule-in non-STEMI only in a specific ACS population.

The early and accurate diagnosis of acute myocardial infarction (AMI) is an important medical and economic challenge. We aimed to prospectively evaluate the performance of the new European Society of Cardiology rapid 0-hour/3-hour (0 h/3 h) rule out protocol for AMI. We enrolled 2,727 consecutive patients presenting with suspected AMI without persistent ST-segment elevation to the emergency department in a prospective international multicenter study. The final diagnosis was adjudicated by 2 independent cardiologists. The performance of the 0 h/3 h rule out protocol was evaluated using 4 high-sensitivity (primary analysis) and 3 sensitive cardiac troponin (cTn) assays. Acute myocardial infarction was the final diagnosis in 473 patients (17.3%). Using the 4 high-sensitivity cTn assays, the 0-hour rule out protocol correctly ruled out 99.8% (95% [confidence interval] CI, 98.7%-100%), 99.6% (95% CI, 98.5%-99.9%), 100% (95% CI, 97.9%-100%), and 100% (95% CI, 98.0%-100%) of late presenters (>6 h from chest pain onset). The 3-hour rule out protocol correctly ruled out 99.9% (95% CI, 99.1%-100%), 99.5% (95% CI, 98.3%-99.9%), 100% (95% CI, 98.1%-100%), and 100% (95% CI, 98.2%-100%) of early presenters (<6 h from chest pain onset). Using the 3 sensitive cTn assays, the 0-hour rule out protocol correctly ruled out 99.6% (95% CI, 98.6%-99.9%), 99.0% (95% CI, 96.9%-99.7%), and 99.1% (95% CI, 97.2%-99.8%) of late presenters; and the 3-hour rule out protocol correctly ruled out 99.4% (95% CI, 98.3%-99.8%), 99.2% (95% CI, 97.3%-99.8%), and 99.0% (95% CI, 97.2%-99.7%) of early presenters. Overall, the 0 h/3 h rule out protocol assigned 40% to 60% of patients to rule out. None of the patients assigned rule out died during 3-months follow-up. The 0 h/3 h rule out protocol seems to allow the accurate rule out of AMI using both high-sensitivity and sensitive cTn measurements in conjunction with clinical assessment. Additional studies are warranted for external validation.

The History, Electrocardiogram, and Troponin (HET) score is a simplified alternative to the HEART score for risk stratifying emergency department (ED) patients with chest pain. This study evaluates the safety and efficacy of the HET score for 30-day cardiac death or myocardial infarction (MI). We conducted a secondary analysis of the STOP-CP multisite cohort study. Risk score components were determined prospectively by the treating provider. Patients were classified into low-, intermediate-, and high-risk strata based on HEART and HET scores. Negative predictive value (NPV) was calculated for the primary safety outcome of cardiac death or MI at 30 days. Consistent with prior studies, the commonly accepted threshold of NPV ≥ 99 % was used to define safety. Efficacy was the proportion of patients classified as low risk. NPV and efficacy were compared between HET and HEART scores using generalized score statistic and McNemar's test, respectively. Among 1460 patients, 46.3 % (676/1460) were women and the mean age was 57.6 ± 12.8 years. Cardiac death or MI at 30 days occurred in 12.7 % (186/1460). Among patients with a low-risk HET score, 1.4 % (4/286) experienced 30-day cardiac death or MI, while 2.2 % (12/534) of patients with a low-risk HEART score had 30-day cardiac death or MI. This yielded a NPV for 30-day of 98.6 % (95 % CI 96.5–99.6 %) for the HET score vs 97.8 % (95 % CI 96.1–98.8 %) for the HEART score (p = 0.29).Efficacy of the HET score was 19.6 % (286/1460, 95 % CI 17.6–21.6 %) vs 36.6 % (534/1460, 95 % CI 34.1–39.1 %) for the HEART score (p < 0.001). In a multisite US cohort study, neither the HET score nor the HEART score achieved a safe NPV. The HET score had significantly lower efficacy than the HEART score. Trial Registration: High-Sensitivity Cardiac Troponin T to Optimize Chest Pain Risk Stratification (STOP-CP; ClinicalTrials.gov: NCT02984436; https://clinicaltrials.gov/ct2/show/NCT02984436).

Chronic kidney disease (CKD) patients with chest pain (CP) should receive special attention in the emergency department (ED). Evaluating troponin levels is highly confusing. This study aims to compare Cystatin C (CysC) and creatinine on troponin results in CKD patients with CP in ED. A prospective cross-sectional study was conducted on 174 patients with CKD who were admitted to ED with CP and registered with clinicaltrials.gov (NCT05303441). Patients were risk classified. Blood samples were collected for 0th-hour, 1st-hour, and 3rd-hour troponin levels and admission CysC level. Then they were grouped as they were diagnosed with ACS or not. CKD-EPI formula was used to calculate Glomerular filtration rate (GFR) with creatinine, CysC and cyscrea for each patient (https://www.kidney.org/professionals/kdoqi/gfr_calculator). The overall rate of CKD stage change calculated with creatinine to another stage with CysC was 52.87 % in all groups. There was a highly significant correlation between creatinine and CysC levels with 1st-hour and 3rd-hour troponin levels in both ACS and non-ACS groups (r = 0.809 and 0.810, respectively; r = 0.908 and 0.912, respectively). The prediction equations between creatinine, CysC, and troponin were as 0th-hour troponin = 1.553 + 1.074creatinine and 0th-hour troponin = 1.580 + 0.837cystatin C, respectively. 3rd-hour troponin level had a markedly good predictive power for ACS (AUC = 0.813, p < 0.001; sensitivity 74.7 %, specificity 74.7 %) with a cut-off value of 64.50. CysC can be preferable in CKD patients with CP due to the stage change and the decisive effect of CysC on troponin compared to creatinine in patients with and without ACS.

ObjectiveTo evaluate the incidence of major adverse cardiac events (MACE) at 1 year in emergency department (ED) patients with possible acute coronary syndromes, stratified by high sensitivity troponin (hs-cTnI) concentrations using sex-specific cut points compared with overall cut points.MethodsIn a multicentre observational study of 2841 patients, presentation hs-cTnI concentrations were categorised using sex-specific (women 16 ng/L; men 34 ng/L) and overall (26 ng/L) cut points. The primary outcome was MACE occurring within 1 year of presentation. Patients with hs-cTnI values concentrations within these categories were reported by sex and 1-year MACE. Net reclassification improvement (NRI) was computed to measure the change in prediction after altering the hs-cTnI cut points, and was calculated separately for events and non-events.ResultsApplication of sex-specific 99th percentile cut points rather than the overall cut point of 26 ng/L, reclassified 25 females from having a non-elevated troponin to having an elevated troponin, and 29 males from having an elevated troponin value to having a non-elevated troponin value on presentation. Of these, 7 (28.0%) females and 12 (41.4%) males had a 1-year MACE. There was no reclassification improvement for those with or without 1-year MACE (NRIevents=−1.5%, 95% CI −4.0% to 1.1%; NRInon-events −0.04%, 95% CI −0.5% to 0.4%).ConclusionsSex-specific cut points improve the identification of women but not men at risk for 1-year MACE. The net-effect across the whole ED population with possible cardiac chest pain is minimal. Lowering the clinical cut point for both sexes may be appropriate for prognostic purposes.Trial registration numberISRCTN No. 21109279, ACTRN12609000283279.