Patients with acute PE and hsTnT ≥73 ng/l had a 6.22-fold higher 30-day MI risk (2.6% vs 0.4%) compared to lower quartiles, p=0.01.
Does a high concentration of high-sensitivity troponin-T predict early myocardial infarction in patients with acute pulmonary embolism without known coronary artery disease?
In patients with acute pulmonary embolism without known coronary artery disease, the risk of early myocardial infarction is very low and primarily confined to those presenting with the highest hsTnT concentrations (≥73 ng/l).
Tasa de eventos absoluta: 0% vs 0%
Abstract Background High-sensitivity cardiac troponins are the gold-standard biomarkers for diagnosing myocardial injury. We have previously shown that elevated high-sensitivity troponin-T (hsTnT) is associated with both short- and long-term mortality in patients with acute pulmonary embolism (PE). However, it is unknown whether hsTnT may reflect a concurrent or emerging acute myocardial infarction (MI) in this setting. Purpose To determine the early risk of MI in individuals with acute PE according to their hsTnT concentration at presentation. Methods Retrospective cohort study based on Danish nationwide administrative registries. We identified all patients discharged from the hospital with a PE from 2013 through 2020 (International Classification of Diseases, Tenth Revision diagnostic codes: I260, I269, and I269A) and merged them with all records of at least one hsTnT (99th percentile upper reference limit, 13.5 ng/l) measurement obtained during the same hospitalization. Subjects with known coronary artery disease (including previous PCI or CABG) were excluded. Persons were stratified into quartiles (Q1-Q4; Figure) based on their first hsTnT measurement. Standardized absolute and relative risks for MI at days 0-30 were calculated through multivariable Cox regression with average treatment effect modeling. Models were standardized for demographic and clinical features, including hemoglobin concentration and estimated glomerular filtration rate. Results A total of 4902 individuals fulfilled the inclusion and exclusion criteria. Median age (25th-75th percentile) was 69.9 (56.8-78.3) years, 2474 (50.5%) were women, and 117 (2.4%) had a prior history of venous thromboembolism. Median baseline hsTnT was 27 (25th-75th percentile, 13-74) ng/l, and 3675 (75.0%) had an elevated concentration. Forty-five (0.9%) individuals had been diagnosed with an MI at 30 days; 29 within the first day of admission, and 16 from days 2 through 30. The cumulative incidence of MI according to each hsTnT quartile is shown in the Figure. Only one MI occurred in Q1, 5 in Q2, 9 in Q3, and 30 in Q4. Accordingly, the crude risk of MI was negligible in Q1 and highest in Q4. The risk in Q4 remained significantly higher upon multivariable adjustment when compared with the other three quartiles combined (Q4 vs. Q1-3; standardized absolute risk 2.6% vs. 0.4%; standardized relative risk 6.22, 95% confidence interval 2.20 to 10.25; p=0.01). Conclusions The risk of early MI was very low in individuals with acute PE who did not have a history of coronary artery disease. Most cases of MI appeared concomitantly with the PE event and in individuals with a hsTnT concentration ³73 ng/l. Indeed, only patients in this highest hsTnT quartile had a significantly higher risk of MI. Because the total number of events was very small, the overall high mortality in this group is unlikely to be driven by unstable coronary artery disease alone.
Frary et al. (Sat,) reported a other. Patients with acute PE and hsTnT ≥73 ng/l had a 6.22-fold higher 30-day MI risk (2.6% vs 0.4%) compared to lower quartiles, p=0.01.