Detection of cardiac troponin I early after onset of chest pain in six patients.

Patients presenting to the emergency departments (ED) with symptoms of acute coronary syndrome (ACS) and with a nondiagnostic electrocardiogram (ECG) pose a management challenge (1). Cardiac troponins [(cTns), tropinin I (cTnI) and tropinin T [cTnT)], creatine kinase (CK), and CK-MB are frequently used in the assessment of ACS. cTns are superior in their analytical specificity and diagnostic sensitivity and specificity for myocardial injury (2, 3). Findings from both animal and clinical studies show that cTnI is released into the blood in various cardiac conditions, including angina, acute myocardial infarction (1, 4, 5), congestive heart failure (6), and myo-carditis (7). Because cTns in serum represent myocardial damage and increased risk of future adverse outcomes (8), improving the detection of serum cTns has implications for better diagnosis of myocardial damage and better risk stratification for patients with ACS. With current clinical assays, cTns are detectable in the circulation 4 – 6 h after the onset of pain in acute myocar-dial infarction, peaking within 12–24 h and remaining increased for a few days (9). However, a recently developed Western blot method, WB-DSA (10), detected minute amounts of cTnI in serum of patients undergoing bypass surgery within 10 min after reperfusion (11), suggesting increased detection of TnI by the WB-DSA method. Although WB-DSA does not permit analysis of troponin's quaternary structure, it does allow accurate assessment of the chemical status of individual troponin subunits, such as the extent and pattern of cTnI degradation. cTnI is specifically degraded in ischemic/reperfused injured rat myocardium (4, 12), and TnI degradation products are detected in myocardium of patients undergoing coronary artery bypass surgery. Because ACS represents a spectrum of cardiac pathophysiology, unique patterns of cTnI degradation may be present in serum at various points along this spectrum and detectable by the WB-DSA. This study presents a series of cases to evaluate the potential clinical applicability of this novel method for the detection of cTnI and any of its degradation products in serum from patients presenting for emergency medical care with symptoms of ACS. Serum samples were obtained from patients presenting within 4 h of onset of symptoms of ACS to the Kingston General Hospital ED. We recruited patients between May and August 2000 and selected those with no or mild increases in CK, CK-MB, or cTnI as measured by clinical methods. Patients were excluded if they had renal impairment or skeletal injury. Patient selection was meant to be …