Lobo, R

Abstract Background Diagnosing myocardial infarction (MI) in patients with chronic kidney disease (CKD) is difficult as these patients often have elevated baseline high-sensitivity cardiac troponin T (hs-cTnT) concentrations. Methods Observational U.S. cohort study of emergency department (ED) patients undergoing hs-cTnT measurement. Cases with >1 hs-cTnT increase >99th percentile were adjudicated following the Fourth Universal Definition of MI. Diagnostic performance of baseline and serial 2- and 6-hour hs-cTnT thresholds for ruling-in acute MI was compared between those without and with CKD (eGFR <60 ml/min/1.73m2). Results The study cohort included 1992 patients, amongst whom 501 (25%) had CKD. There were 701 (82%) patients with myocardial injury, 64 (7.5%) with type 1, and 91 (11%) with type 2 MI. In CKD patients with baseline hs-cTnT thresholds of >52, >100, >200 or >300 ng/L, PPVs for acute MI were 37% [95% CI 28-46], 53% (95% CI 39-67), 73% (95% CI 50-89) and 80% (95% CI 44-98), and in those without CKD, 64% (95% CI 50-77), 69% (95% CI 49-85), 59% (95% CI 33-82) and 54% (95% CI 25-81). In CKD patients with a 2-hour hs-cTnT delta of >10, >20 or >30 ng/L, the corresponding PPVs were 65% (95% CI 50-78), 86% (95% CI 68-96) and 88% (95% CI 68-97), and in those without CKD, 65% (95% CI 51-78), 73% (95% CI 57-86) and 75% (95% CI 58-88) (Figure). Conclusion Diagnostic performance of standard baseline and serial 2-hour hs-cTnT thresholds to rule-in MI is suboptimal in patients with CKD. It significantly improves when using higher baseline thresholds and delta values.

Abstract Background Artificial intelligence-augmented electrocardiogram (AI-ECG) algorithms have been developed from the standard 12-lead ECG and validated for the recognition of left ventricular systolic dysfunction (LVSD), defined as LV ejection fraction (LVEF)≤35%. Whether AI-ECG facilitates identification of LVSD and is associated with adverse outcomes in emergency department (ED) patients undergoing high-sensitivity cardiac troponin (hs-cTnT) testing is uncertain. Purpose To investigate the diagnostic and prognostic performance of AI-ECG in ED patients undergoing hs-cTnT measurement. Methods Observational US cohort study of ED patients undergoing hs-cTnT measurement. Cases with hs-cTnT increases >sex-specific 99th percentiles were adjudicated following the Fourth Universal Definition of Myocardial Infarction (MI). Post-discharge major adverse cardiac events (MACE) included death, MI, heart failure (HF) hospitalization, stroke or transient ischemic attack, and new onset atrial fibrillation/flutter during 2-years follow-up. The AI-ECG network output, which is a continuous number between 0–1, that provides a probability of LVSD, was obtained for each patient from the first ECG during the index presentation. An AI-ECG threshold of ≥0.256 indicates a positive screen that correlates with a high probability of LVSD. Results Among 1977 patients, 1729 (87%) had a negative AI-ECG screen, while 248 (13%) had a positive AI-ECG screen. Patients with a positive AI-ECG screen were older and had more comorbidities. As compared to patients with hs-cTnT≤99th percentile in whom AI-ECG was positive in 5.8%, those with hs-cTnT>99th percentile had a positive AI-ECG in 22% of cases (p<0.0001). Based on adjudicated diagnoses, the frequency of a positive AI-ECG was 20% in myocardial injury, 38% in type 1 MI, and 20% in type 2 MI. At 2-years follow-up, as compared to patients with a negative AI-ECG, those with a positive AI-ECG had a higher risk for MACE (48% vs. 21%, p<0.0001, adjusted HR 1.39, 95% CI 1.11–1.75) (Figure 1), mainly because of more deaths (43% vs. 30%, p=0.004) and HF hospitalizations (36% vs. 13%, p<0.0001). A positive AI-ECG was associated with a higher risk for MACE (60% vs. 41%, p<0.0001, adjusted HR 1.30, 95% CI 1.02–1.64) in those with hs-cTnT increases >99th percentile, but not in those without hs-cTnT increases. Among patients with an echocardiogram during index presentation or within 30-days (n=452), the diagnostic accuracy of AI-ECG for LVEF ≤35% was 81.4% (95% CI 77.5, 84.9) with a negative predictive value of 96.5% (95% CI 94.0, 98.2). A normal LVEF (>50%) was observed in 87% of those with a negative AI ECG, whereas in those with a positive AI-ECG LVEF was reduced (<50%) in 60%. Conclusions Among ED patients evaluated with hs-cTnT, a positive AI-ECG screen for LVSD identifies patients at high risk of MACE. These findings are largely because of more deaths and HF hospitalizations in those with hs-cTnT increases >sex-specific 99th percentiles. Funding Acknowledgement Type of funding sources: None.

Abstract Background and introduction Cardioversion is commonly used to terminate cardiac arrhythmias. Some previous reports have suggested that cardioversion results in myocardial injury as evidenced by increased levels of cardiac troponin. However, many of these studies were done years ago with less sensitive troponin assays and monophasic waveform defibrillators. Purpose To determine if external direct current (DC) cardioversion with biphasic rectilinear waveform shocks results in myocardial injury as assessed by high sensitivity cardiac troponin T (hs-cTnT) and I (hs-cTnI). Methods Patients scheduled for elective DC cardioversion for atrial fibrillation or atrial flutter were recruited. Plasma samples for measurement of hs-cTnT and hs-cTnI were obtained pre-cardioversion and as late as feasible but at least 6 hours post-cardioversion [median of 9 (7–11) hours]. Results A total of 96 patients were recruited. One patient was excluded because the pre-cardioversion sample was hemolysed. Median (25th–75th interquartile range) cumulative energy delivered was 121.6J (62.4–277.4J) and median highest energy individual shock was 121.0J (62.1–146.2J). A total of 39 (41.1%) patients received more than 1 shock, 23 (24.2%) patients received a cumulative energy of 300J or higher and 5 (5.3%) patients received a cumulative energy of 1,000J or more. The median pre-cardioversion hs-cTnT value was 11.48 (7.19–18.38) ng/L and the median hs-cTnI value was 5.1 (2.0–9.4) ng/L. Median post-cardioversion hs-cTnT value were 12.46 (7.98–20.28) ng/L and hs-cTnI value were 6.3 (3.5–10.0) ng/L. Wilcoxon-Signed ranks test showed a statistically significant change between the pre-and-post cardioversion hs-cTnT values (Z=−4.237, p<0.001) and hs-cTnI values (Z=−4.822, p<0.001). In only 5 (hs-cTnT) and 4 patients (hs-cTnI) was there an increase of >5 ng/L. There were 5 cases where the post-cardioversion values of both hs-cTnT and hs-cTnI were above the 50% reference change value. There was no relation between the change in hs-cTn values and sex, number of shocks, total energy delivered (even in those who received more than 1,000J), highest energy per shock, total current delivered, highest current delivered per shock or transthoracic impedance. Conclusion(s) There is a statistically significant but very small change in median hs-cTnT and hs-cTnI values (1 ng/L and 1.2 ng/L respectively) after DC cardioversion. The results were similar even in patients where high energy shocks were delivered and did not vary based on the pre cardioversion baseline value. Patients who have marked troponin elevations after cardioversion should be assessed for other causes of myocardial injury. It should not be assumed that they have myocardial injury from the cardioversion alone. Figure 1 Funding Acknowledgement Type of funding source: Other. Main funding source(s): Dr. Allan Jaffe has substantial research funds from both grants and private industry. Funds were used to pay for blood sample collection and analysis of high sensitivity cardiac troponin T at Mayo Clinic. Abbott Laboratories donated reagents for the high sensitivity cardiac troponin I analysis.