Performance of Multiple Cardiac Biomarkers Measured in the Emergency Department in Patients with Chronic Kidney Disease and Chest Pain

• Published in: Academic emergency medicine 2002-12, Vol.9 (12), p.1389-1396
• Main Authors: McCullough, Peter A., Nowak, Richard M., Foreback, Craig, Tokarski, Glenn, Tomlanovich, Michael C., Khoury, Nabil E., Weaver, W. Douglas, Sandberg, Keisha R., McCord, James
• Format: Article
• Language: English
• Subjects: cardiac markers; chest pain; chronic renal disease; creatine kinase; diagnosis; dialysis; myoglobin; tropoinin I
• ISSN: 1069-6563; 1553-2712
• DOI: 10.1197/aemj.9.12.1389

Objective: To evaluate the individual components of a cardiac multimarker panel in the detection of acute myocardial infarction (AMI) in patients with chest pain across a spectrum of renal dysfunction. Methods: A total of 817 consecutive patients evaluated for a possible AMI in the emergency department (ED) enrolled in a prospective study of cardiac biomarkers assessed using a point‐of‐care device with myoglobin (MYO), cardiac troponin I (cTnI), and creatine kinase myocardial band (CK‐MB), recorded at 0, 1.5, 3, and 9 hours. This study did not exclude patients on the basis of renal dysfunction. Baseline renal function was available in 808 patients. Patients were stratified by corrected creatinine clearance (CorrCrCl) into quartiles, and those on dialysis (n = 51) were considered as a fifth comparison group. Those patients with advanced renal dysfunction (CorrCrCl < 47/mL/min/72 kg) or on dialysis had higher rates of diabetes, hypertension, and prior coronary disease. Agreement for the diagnosis of AMI was required of two independent cardiologists using criteria based on history, electrocardiogram, and central laboratory assessment of serial cardiac markers. Results: More than 99% of all patients were admitted to a chest pain observation unit or the hospital. Mean MYO levels were elevated in the presence of renal dysfunction in those with and without myocardial infarction. Both MYO and CK‐MB were correlated with CorrCrCl, (r = ‐0.36, p < 0.01, and r = ‐0.10, p = 0.01, respectively), while cTnI was not (r = ‐0.10, p = 0.12). Using multiple receiver operating characteristic curve testing, cTnI was found to be the most consistent marker across all strata of renal dysfunction, including end‐stage renal disease on dialysis. The authors did not find a trend for false‐positive cTnI and renal dysfunction. Conclusions: A point‐of‐care, rapid cardiac biomarker strategy utilizing cTnI is applicable and superior to MYO or CK‐MB in the evaluation of chest pain in patients with renal dysfunction.