Abstract 14077: Use of Cardiac Troponin I to Identify Acute Myocardial Infarction in Patients With Impaired Renal Function

Abstract

Introduction: Cardiac troponins are the gold standard to diagnose acute myocardial infarction (AMI). Troponin I (TnI) levels are known to be increased in patients with chronic kidney disease (CKD) irrespective of an AMI. The established diagnostic TnI cut-off to detect AMI is calculated based on a healthy reference population and might not be representative for CKD patients. Hypothesis: The aim of this study was to investigate TnI levels in patients with and without CKD with suspected AMI and to calculate CKD- optimized diagnostic TnI thresholds. Methods: Of 1572 patients enrolled with suspected AMI, 266 patients showed an impaired renal function with estimated glomerular filtration rate (eGFR) of less then 60ml/min and were classified as patients with CKD. N=77 (34%) of patients with CKD and n=278 (24%) without CKD had the final diagnosis AMI. TnI was measured on admission and after 3h. Based on receiver operator characterics curve analyses (AUROC) of the baseline levels CKD optimized TnI threshold were derived. Sensitivity and specifity were calculated for the 99th percentile cut-off (30.0 pg/mL), the optimized cut-off (58.0 pg/mL) and the change in TnI concentration within 3h after admission. Results: Patients with CKD had higher TnI levels then patients without CKD (6.0pg/mL vs. 20.9pg/ml; p<0.001). This difference was more pronounced in patients without AMI (median 9.1 vs. 4.4; p<0.001), whereas the difference diminished in AMI patients (median 337.4 vs. 238.6; p=0.83). In CKD patients TnI remained a strong marker to detect AMI with AUROC of 0.933 compared to 0.969 in patients without CKD. Applying the 99th percentile threshold it was associated with a relevant loss of specificity in CKD patients with 80% compared to 96% in patients without CKD. This poor specificity could be regained by use of a higher CKD-optimized threshold or use of the change in TnI concentration within 3h leading to specificities of 90% and 96%, respectively. Conclusions: Patients presenting with suspected AMI and CKD have higher TnI levels on admission compared to patients without CKD leading to a low specificity detecting AMI in CKD patients. Using an CKD-optimized TnI cut-off level on admission or using the change in TnI concentration within 3h is able to regain this lost specificity.