Serum troponin is often elevated in patients with acute stroke and its mechanism is unknown. In a retrospective single-center cohort study, we evaluated the association between stroke severity and serum troponin in 187 patients with acute stroke using multivariable modified Poisson models. A one-point increase in the National Institutes of Health Stroke Scale (measure of stroke severity) was associated with a marginally higher serum troponin level in adjusted models (aIRR 1.03; 1.01–1.05, P = 0.001). The modest, yet potentially independent, association between stroke severity and serum troponins could suggest a neurogenic basis for a cardiac injury in patients with acute stroke.

Although the cardiovascular benefits of an increased urinary potassium excretion have been suggested, little is known about the potential cardiac association of urinary potassium excretion in patients with chronic kidney disease. In addition, whether the cardiac association of urinary potassium excretion was mediated by serum potassium levels has not been studied yet. We reviewed the data of 1633 patients from a large-scale multicentre prospective Korean study (2011–2016). Spot urinary potassium to creatinine ratio was used as a surrogate for urinary potassium excretion. Cardiac injury was defined as a high-sensitivity troponin T ≥ 14 ng/l. OR and 95 % (CI for cardiac injury were calculated using logistic regression analyses. Of 1633 patients, the mean spot urinary potassium to creatinine ratio was 49·5 (sd 22·6) mmol/g Cr and the overall prevalence of cardiac injury was 33·9 %. Although serum potassium levels were not associated with cardiac injury, per 10 mmol/g Cr increase in the spot urinary potassium to creatinine ratio was associated with decreased odds of cardiac injury: OR 0·917 (95 % CI 0·841, 0·998), P = 0·047) in multivariate logistic regression analysis. In mediation analysis, approximately 6·4 % of the relationship between spot urinary potassium to creatinine ratio and cardiac injury was mediated by serum potassium levels, which was not statistically significant (P = 0·368). Higher urinary potassium excretion was associated with lower odds of cardiac injury, which was not mediated by serum potassium levels.

Two adolescent males presented within 3 days after the first and second dose of the BNT162b2 vaccine with chest pain. Elevated troponin levels, ST segment elevation, and enhancement of the myocardium in cardiac MRI suggested myocarditis. Left ventricular function remained normal, symptoms resolved, and patients were discharged in 4 days. BNT162b2 vaccine may be associated with self-limited myocarditis in youth.

Introduction: Acute myocardial infarction (MI) is one of the most time-sensitive diagnoses made in the emergency department (ED). Troponin (TNI) measurement is an invaluable tool; however, its utility depends on the clinical context and is highest where there is a strong pre-test probability. Studies show that most TNI elevations are due to non-cardiovascular causes; however, elevated TNI has been associated with increased morbidity and mortality, often prompting additional investigations. The aim of our study was to compare 1-year cardiac outcomes of patients who presented to the ED with non-cardiac complaints and elevated TNI who had further cardiac testing versus those who did not. Methods: We conducted a retrospective chart review of patients ≥18 seen in the ED for non-cardiac complaints with a high TNI from January-June 2016. Patients were stratified into two groups: 1) those who received diagnostic testing for ischemia and/or a cardiac consultation and 2) those without cardiac consultation or testing. Data was also collected on major adverse cardiac events within 1-year of ED presentation. Chi-squared analysis assessed the difference in proportions of outcomes between groups. We present our preliminary data. Results: In total, 1500 patients met inclusion criteria and 861 have been analyzed thus far. Of these 861, 209 went on to have either diagnostic testing for ischemia and/or a cardiology consult while 652 had no further investigations. There was no statistically significant difference in the proportion of patients who developed unstable angina (p = 0.9824), ST-elevation myocardial infarction (STEMI) (p = 0.9956), non-STEMI (p = 0.9008), stroke/TIA (p = 0.9657), revascularization (p = 0.8873), cardiac hospitalization (p = 0.9446) or died (p = 0.8972), within 1-year of their ED presentation. Conclusion: In patients with isolated elevated TNI and non-cardiac complaints, preliminary data showed no difference in mortality or cardiac event rates between those who had further testing/consultations and those who did not. TNI ordering could be cautiously limited to only presenting complaints/preliminary diagnoses likely to have cardiac etiology or sequelae or those in whom further testing would impact management/outcomes. Quality of care may be improved by reducing length of stay in the ED and potential risks of unnecessary tests. Future studies include determining cost implications and classifying what level of TNI elevation in non-ACS patients may predict a future cardiac outcome.

Troponin levels are often obtained when chest pain is evaluated in the paediatric emergency department. Elevations in troponin levels can be due to different causes, and it is important to fully understand all of these possible causes to help streamline further evaluation and therapy. We present the case of a teenager who had two episodes of troponin elevation in the setting of rhabdomyolysis.

Introduction: Our team developed “The Ottawa Troponin Pathway” (OTP) for Non-ST Elevation Myocardial Infarction (NSTEMI) diagnosis using serial conventional troponin (cTnI) 3 hours apart to aid in safe and early disposition of ED patients. The primary objective of this study is to validate the diagnostic accuracy of the OTP in the cohort of patients with cTnI values above the 99th percentile ( > 45ng/L). Methods: This study is a health records review conducted at the Civic and General Campuses of The Ottawa Hospital from August 2017 to December 2017. Adults (≥18 years) who presented to the ED with symptoms of ACS, and who had serial cTnI (at least two values 3 hours ±15 minutes apart) performed for diagnosis of NSTEMI and at least one cTnI value > 45ng/L were included. Patients with cardiac arrest, STEMI, unstable angina or those with TnI values ≤45ng/L were excluded. The outcomes were death due to unknown cause or NSTEMI adjudicated by two blinded investigators within 30 days. Data collected include baseline characteristics, ED management, length of stay, cTnI values and times of measurement, disposition, and outcome. We used descriptive statistics and test diagnostic characteristics to analyze our data. Results: We screened 53,077 patients, of whom 635 patients were included in the study (mean age 71.6 years; 57.6% males; 59.7% hospitalized; median ED length of stay 4.7 hours.). 107 patients (16.9%; 95%CI 14.1%-20.0%) were diagnosed with NSTEMI within 30 days. Among patients with TNI values above the 99th percentile, the OTP did not miss any patients diagnosed with NSTEMI. The sensitivity and the specificity of the OTP were 100% (95%CI 96.6%-100%) and 32.2% (95%CI 28.2%-36.4%) respectively. Conclusion: Our results show that the OTP is diagnostically accurate in ruling out NSTEMI among patients with cTNI values above the 99th percentile with symptoms concerning for ACS. Using the OTP will allow for early referral to consulting services for management, safe and early discharge home, and improve ED crowding.

Introduction: Very low concentrations of high-sensitivity cardiac troponin can rule-out myocardial infarction (MI) at ED arrival in patients with chest pain. However, this single troponin rule-out strategy works poorly in patients with renal impairment and elevated baseline troponin levels. The objective of this study was to develop and validate a troponin adjustment strategy to accurately rule-out MI with a single hs-cTnTmeasurement in patients with kidney dysfunction. Methods: We used data from three cohorts of ED chest pain patients to develop an adjustment score for a high-sensitivity troponin T (hs-cTnT) assay in patients with kidney dysfunction. The derivation cohort (n = 8846) used administrative and registry data. Two validation cohorts (n = 1187 and 1092) were prospectively-collected. The score assigned points for increasing hs-cTnT levels and subtracted points for lower estimated glomerular filtration rate (eGFR). In the derivation cohort, hs-cTnT concentrations achieving 98.5% sensitivity in of patients with eGFR ≥60, 45-59, 30-44, 15-29 and <15 were assigned ascending positive integer values. Negative integer values were assigned to eGFR values 45-59, 30-44, 15-29 and <15. The scpres for troponin and eGFR were summed for each patient, with scores ranging from −4 to +5. The proportion of patients with 7-day MI ruled out by a score ≤0, sensitivity, NPV, negative likelihood ratio (LR-) and area under the curve (AUC) were quantified in each study cohort. Results: The derivation and validation cohorts had 7-day MI rates of 5.7, 8.6 and 9.1%. In the derivation cohort, a score ≤0 ruled out MI in 35% of patients, with a sensitivity for 7-day MI of 99.5% (95% CI 98-100), NPV of 99.9% (95% CI 98.4-99.9), LR- of 0.02 (95% CI 0.01-0.05) and AUC of 0.88. In the first validation cohort, a score ≤0 ruled out MI in 45% of patients, with a sensitivity for 7-day MI of 97% (95% CI 90-100%), NPV of 99% (95% CI 98-100%), LR- 0.06 (0.02-0.18) and AUC of 0.89. In the second validation cohort, a score ≤0 ruled out MI in 20% of patients, with a sensitivity for 7-day MI of 96% (95% CI 93-99%), NPV of 98% (95% CI 96-100%), LR- of 0.16 (95% CI 0.07-0.39) and AUC of 0.78. Conclusion: We developed and validated a simple scoring system to adjust hs-cTnT concentrations for a patient's kidney function that enables MI to be ruled out in a large proportion of chest pain patients using a single measurement on ED presentation.

Introduction: Guidelines recommend serial conventional cardiac troponin (cTn) measurements 6-9 hours apart for non-ST-elevation myocardial infarction (NSTEMI) diagnosis. We sought to develop a pathway based on absolute/relative changes between two serial conventional cardiac troponin I (cTnI) values 3-hours apart for 15-day MACE identification. Methods: This was a prospective cohort study conducted in the two large ED's at the Ottawa Hospital. Adults with NSTEMI symptoms were enrolled over 32 months. Patients with STEMI, hospitalized for unstable angina, or with only one cTnI were excluded. We collected baseline characteristics, Siemens Vista cTnI at 0 and 3-hours after ED presentation, disposition, and ED length of stay (LOS). Adjudicated primary outcome was 15-day MACE (AMI, revascularization, or death due to cardiac ischemia/unknown cause). We analysed cTnI values by 99th percentile cut-off multiples (45, 100 and 250ng/L). Results: 1,683 patients (mean age 64.7 years; 55.3% female; median ED LOS 7 hours; 88 patients with 15-day MACE) were included. 1,346 (80.0%) patients with both cTnI ≤45ng/L; and 58 (3.4%) of the 213 patients with one value≥100ng/L but both <250ng/L or ≤20% change did not suffer MACE. Among 124 patients (7.4%) with one value >45ng/L but both <100ng/L based on 3 or 6-hour cTnI, one patient with Δ<10ng/L and 6 of 19 patients with Δ≥20ng/L were diagnosed with NSTEMI (patients with Δ10-19ng/L between first and second cTnI had third one at 6-hours). Based on the results, we developed the Ottawa Troponin Pathway (OTP) with a 98.9% sensitivity (95%CI 96.7-100%) and 94.6% specificity (95%CI 93.4-95.7%). Conclusion: The OTP, using two conventional cTnI measurements performed 3-hours apart, should lead to better identification of NSTEMI particularly those with values >99th percentile cut-off, standardize management and reduce the ED LOS.

Introduction: ex-specific diagnostic cutoffs may improve the test characteristics of high-sensitivity troponin assays for the diagnosis of myocardial infarction. Sex-specific cutoffs for ruling in MI improve the sensitivity of the assay for MI among women, and improve the specificity of diagnosis among men. We hypothesized that the use of sex-specific high-sensitivity Troponin T (hsTnT) cutoffs for ruling out MI at the time of ED arrival would improve the classification efficiency of the assay by enabling more patients to have MI ruled out at the time of ED arrival while maintaining diagnostic sensitivity. The objective of this study was to quantify the test characteristics of sex-specific cutoffs of an hsTnT assay for acute myocardial infarction (AMI) when performed at ED arrival in patients with chest pain. Methods: This retrospective study included consecutive ED patients with suspected cardiac chest pain evaluated in four urban EDs were, excluding those with ST-elevation AMI, cardiac arrest or abnormal kidney function. The primary outcomes was AMI at 7 days. Secondary outcomes included major adverse cardiac events (MACE: all-cause mortality, AMI and revascularization) and the individual MACE components. We quantified test characteristics (sensitivity, negative predictive value, likelihood ratios and proportion of patients ruled out) for multiple combinations of sex-specific rule-out cutoffs. We calculated net reclassification improvement compared to universal rule-out cutoffs of 5ng/L (the assays limit of detection) and 6ng/L (the FDA-approved limit of quantitation for US laboratories). Results: 7130 patients, including 3931 men and 3199 women, were included. The 7-day incidence of AMI was 7.38% among men and 3.78% among women. Universal cutoffs of 5 and 6 ng/L ruled out AMI with 99.7% sensitivity in 33.6 and 42.2% of patients. The best-performing combination of sex-specific cutoffs (8g/L for men and 6ng/L for men) ruled out AMI with 98.7% sensitivity in 51.9% of patients. Conclusion: Sex-specific hsTnT cutoffs for ruling out AMI at ED arrival may achieve substantial improvement in classification performance, enabling more patients to be ruled out at ED arrival, while maintaining acceptable diagnostic sensitivity for AMI. Universal and sex-specific rule-out cutoffs differ by only small changes in hsTnT concentration. Therefore, these findings should be confirmed in other datasets.

Introduction: Patients with chronic kidney disease (CKD) are at high risk of cardiovascular events, and have worse outcomes following acute myocardial infarction (AMI). Cardiac troponin is often elevated in CKD, making the diagnosis of AMI challenging in this population. We sought to quantify test characteristics for AMI of a high-sensitivity troponin T (hsTnT) assay performed at emergency department (ED) arrival in CKD patients with chest pain, and to derive rule-out cutoffs specific to patient subgroups stratified by estimated glomerular filtration rate (eGFR). We also quantified the sensitivity and classification performance of the assays limit of detection (5 ng/L) and the FDA-approved limit of quantitation (6 ng/L) for ruling out AMI at ED arrival. Methods: Consecutive patients in four urban EDs from the 2013 calendar year with suspected cardiac chest pain who had a Roche Elecsys hsTnT assay performed on arrival were included f. This analysis was restricted to patients with an eGFR< 60 ml/min/1.73m2. The primary outcome was 7-day AMI. Secondary outcomes included major adverse cardiac events (death, AMI and revascularization). Test characteristics were calculated and ROC curves were generated for eGFR subgroups. Results: 1416 patients were included. 7-day AMI incidence was 10.1%. 73% of patients had an initial hsTnT concentration greater than the assays 99th percentile (14 ng/L). TCurrently accepted cutoffs to rule out MI at ED arrival ( 5 ng/L and 6 ng/L) had 100% sensitivity for AMI, but no patients with an eGFR less than 30 ml/min/1.73M had hsTnT concentrations below these thresholds. We derived eGFR-adjusted cutoffs to rule out MI with sensitivity >98% at ED arrival, which were able to rule out 6-42% of patients, depending on eGFR category. The proportion of patients able to be accurately ruled-in with a single hsTnT assay was substantially lower among patients with an eGFR <30 ml/min/1.73m2 (6-20% vs 25-43%). We also derived eGFR-adjusted cutoffs to rule-in AMI with specificity >90%, which accurately ruled-in up to 18% of patients. Conclusion: Cutoffs achieving acceptable diagnostic performance for AMI using single hsTnT sampling on ED arrival may have limited clinical utility, particularly among patients with very low eGFR. The ideal diagnostic strategy for AMI in patients with CKD likely involves serial high-sensitivity troponin testing with diagnostic thresholds customized to different eGFR categories.

Introduction: Chest pain is one of the most common presenting complaints to emergency departments (EDs) across the world, and the exclusion of acute myocardial infarction (AMI) using troponin testing is central to the care of many of these patients. Testing strategies using conventional troponin assays require repeat testing over many hours to avoid missed diagnoses. This study aims to validate the ability of very low concentrations of troponin at presentation to exclude AMI in ED chest pain patients. Methods: This prospective cohort study was conducted at a single urban tertiary centre and regional percutaneous coronary intervention site in Calgary, Alberta. Patients were eligible for enrolment if they presented to the ED with chest pain, were 25-years or older and required biomarker testing to rule out AMI at the discretion of the attending emergency physician. Patients were excluded if they had clear acute ischemic ECG changes, new arrhythmia or renal failure requiring hemodialysis. High-sensitivity troponin-T (Roche Elecsys hs-cTnT) results were obtained in all patients at presentation. Relevant outcomes were obtained from administrative data. The primary outcome was AMI within 30-days of ED visit, the secondary outcome was 30-day major adverse cardiac events (MACE). The study was REB approved. Results: A total of 1,016 patients were enrolled from August 2014-September 2016, of which 174 (17.1%) patients had an initial troponin below the limit of blank (<3 ng/L) and 369 (36.3%) had a level below the limit of detection (<5 ng/L). The sensitivity and negative predictive value (NPV) of a troponin below limit of blank (<3 ng/L) for 30-day AMI were 100% (95% CI 89.3%-100%) and 100% (95% CI 97.8-100%), respectively. The sensitivity and NPV of a troponin below limit of detection (<5 ng/L) for 30-day AMI were 93.8% (95% CI 80.0-98.3%) and 99.5% (95% CI 98.1-99.9%) respectively. Sensitivity for 30-day MACE at both cutoffs was lower: 96.1% (95% CI 92.5-98.0%) for <3 ng/L, and 88.4% (95% CI 83.3-92.1%) for <5 ng/L, respectively. Conclusion: A high sensitivity troponin T result below the limit of blank is highly sensitive at excluding AMI and identifies patients at reasonably low risk of 30-day MACE. A result below the limit of detection will identify a larger population of patients as low risk but has a greater risk of missed AMI and MACE.

Introduction: The HEART score is a validated tool created to risk stratify emergency department (ED) chest pain patients using 5 simple criteria (History, ECG findings, Age, Risk factors, and Troponin). Several studies have demonstrated the superiority of HEART over other well known risk stratification tools in identifying low risk chest pain patients suitable for early discharge. All but one of these studies used conventional troponin assays, and most were conducted in European populations. This study aims to validate the HEART score using a high-sensitivity troponin T assay in a Canadian population. Methods: This prospective cohort study was conducted at a single urban tertiary centre and regional percutaneous coronary intervention site in Calgary, Alberta. Patients were eligible for enrolment if they presented to the ED with chest pain, were age 25-years or older and required biomarker testing to rule out AMI at the discretion of the attending emergency physician. Patients were excluded if they had clear acute ischemic ECG changes, new arrhythmia or renal failure requiring hemodialysis. Clinical data were recorded by the emergency physician at the time of enrolment and outcomes were obtained from administrative data. High-sensitivity troponin-T (Roche Elecsys hs-cTnT) results were obtained in all patients at presentation. The primary outcome was AMI within 30-days of ED visit, the secondary outcome was 30-day major adverse cardiac events (MACE). Results: A total of 984 ED patients with complete HEART scores were enrolled from August 2014 to September 2016. The 30-day incidence of AMI and MACE in the overall population was 3.3% and 20.6%, respectively. HEART scores were predictive of 30-day AMI incidence: low risk (0-3): 0.77% (95%CI 0.0-1.5%), moderate risk (4-6): 4.3% (95%CI 2.3-6.2%) and high risk (7-10): 12.2% (95%CI 5.5-19.0%). HEART scores also predicted 30-day MACE: low risk (0-3): 5.0% (95%CI 3.1-6.9%), moderate risk (4-6): 31.8% (95%CI 27.2-36.4%) and high-risk (7-10): 61.4% (95%CI 51.2-71.5%). More than half of patients, 522 (53.0%) could be identified as low risk based on the HEART score using a single troponin result. Conclusion: Using a single high-sensitivity troponin result collected at ED presentation, the HEART score can rapidly and effectively identify more than half of ED chest pain patients as low risk for 30-day AMI, but is less sensitive for 30-day MACE.

Introduction: Chest pain and symptoms of acute coronary syndrome are responsible for a large proportion of ED visits and acute hospitalizations. However, only about 15% of patients presenting to the ED with high-risk symptoms do, in fact, have an acute coronary syndrome. The objective of this study is to derive a 2-hour high-sensitivity Troponin T (hsTnT) testing algorithm with outcome based-cutoffs to rapidly rule out acute myocardial infarction (AMI) in a large proportion of ED chest pain patients. Methods: Patients included consecutive ED patients with a chief complaint of cardiac chest pain who had an hsTnT assay performed at ED arrival and 2 hours after ED arrival. Administrative databases were queried to identify troponin results and major adverse cardiac outcomes (MACE) including death, MI, and revascularization. Test characteristics of iterative combinations of initial troponin level and absolute change in troponin level were quantified in order to identify the testing algorithm that identified the greatest proportion of patients eligible for early discharge while maintaining a target sensitivity of 98.5% for the primary outcome of 7-day AMI. Results: 755 eligible patients had hsTnT assays performed at ED arrival and at 2 hours. 91 patients (12.1%) had a 7-day AMI while 108 (14.0%) had 7-day MACE. An initial hsTnT level of less than 14 ng/L, in combination with a 2-hour absolute change of less than 10ng/L had a sensitivity of 98.9% (95% CI 94.0,99.8) and an NPV of 99.8% (95% CI 98.7, 100.0) for 7-day AMI. This identified 58.5% of all patients as being suitable for early discharge. Sensitivity and NPV for 7-day MACE were 90.0% (95% CI 83.3, 94.2) and 97.3% (95% CI 95.3,98.4) respectively. Sex-specific differences in test characteristics were not clinically important. Rule-in hsTnT cutoffs were also evaluated, with specificities ranging from 85-95%, although cutoffs with higher specificity had less ability to rapidly rule-in AMI, leaving more patients with indeterminate results after 2 hours. Conclusion: A hsTnT algorithm can safely and accurately rule out AMI in 58.5% of ED chest pain patients within 2 hours of ED arrival. The lower sensitivity of this algorithm for MACE compared to AMI speaks to the importance of clinical assessment and ECG findings in identifying patients at risk for acute coronary syndromes.